Handouts Available at the Web Site Next Week: www ... Decompensated Heart Failure (ADHF) 9 Common Precipitating Factors of ADHF Non adherence with Medications Dietary sodium intake

Handouts Available at the Web Site Next Week:

www.cardionursing.com

Drawing at the end of todays program.

Sneak peek of our book.

Must be present to win. 1

Presented By

Cynthia Webner DNP, RN, CCNS, CCRN-CMC, CHFN

2 2014 www.cardionursing.com

3

They may forget your

name, but they will never

forget how you made

them feel.

-Maya Angelou

Definitions

4

Definition of Heart Failure

Classification Ejection

Fraction Description

I. Heart Failure with

Reduced Ejection

Fraction (HFrEF)

≤40% Also referred to as systolic HF. Randomized clinical trials have

mainly enrolled patients with HFrEF and it is only in these

patients that efficacious therapies have been demonstrated to

date.

II. Heart Failure

with Preserved

Ejection Fraction

(HFpEF)

≥50% Also referred to as diastolic HF. Several different criteria have

been used to further define HFpEF. The diagnosis of HFpEF is

challenging because it is largely one of excluding other potential

noncardiac causes of symptoms suggestive of HF. To date,

efficacious therapies have not been identified.

a. HFpEF,

Borderline

41% - 49% These patients fall into a borderline or intermediate group. Their

characteristics, treatment patterns, and outcomes appear similar to

those of patient with HFpEF.

b. HFpEF

Improved

>40% It has been recognized that a subset of patients with HFpEF

previously had HFrEF. These patients with improvement or

recovery in EF may be clinically distinct from those with

persistently preserved or reduced EF. Further research is needed

to better characterize these patients. 5

Stages, Phenotypes and Treatment of HF

STAGE AAt high risk for HF but

without structural heart

disease or symptoms of HF

STAGE BStructural heart disease

but without signs or

symptoms of HF

THERAPY

Goals

· Control symptoms

· Improve HRQOL

· Prevent hospitalization

· Prevent mortality

Strategies

· Identification of comorbidities

Treatment

· Diuresis to relieve symptoms

of congestion

· Follow guideline driven

indications for comorbidities,

e.g., HTN, AF, CAD, DM

· Revascularization or valvular

surgery as appropriate

STAGE CStructural heart disease

with prior or current

symptoms of HF

THERAPYGoals· Control symptoms· Patient education· Prevent hospitalization· Prevent mortality

Drugs for routine use· Diuretics for fluid retention· ACEI or ARB· Beta blockers· Aldosterone antagonists

Drugs for use in selected patients· Hydralazine/isosorbide dinitrate· ACEI and ARB· Digoxin

In selected patients· CRT· ICD· Revascularization or valvular

surgery as appropriate

STAGE DRefractory HF

THERAPY

Goals

· Prevent HF symptoms

· Prevent further cardiac

remodeling

Drugs

· ACEI or ARB as

appropriate

· Beta blockers as

appropriate

In selected patients

· ICD

· Revascularization or

valvular surgery as

appropriate

e.g., Patients with:

· Known structural heart disease and

· HF signs and symptoms

HFpEF HFrEF

THERAPY

Goals

· Heart healthy lifestyle

· Prevent vascular,

coronary disease

· Prevent LV structural

abnormalities

Drugs

· ACEI or ARB in

appropriate patients for

vascular disease or DM

· Statins as appropriate

THERAPYGoals· Control symptoms· Improve HRQOL· Reduce hospital

readmissions· Establish patient’s end-

of-life goals

Options· Advanced care

measures· Heart transplant· Chronic inotropes· Temporary or permanent

MCS· Experimental surgery or

drugs· Palliative care and

hospice· ICD deactivation

Refractory symptoms of HF at rest, despite GDMT

At Risk for Heart Failure Heart Failure

e.g., Patients with:

· Marked HF symptoms at

rest

· Recurrent hospitalizations

despite GDMT

e.g., Patients with:

· Previous MI

· LV remodeling including

LVH and low EF

· Asymptomatic valvular

disease

e.g., Patients with:

· HTN

· Atherosclerotic disease

· DM

· Obesity

· Metabolic syndrome

or

Patients

· Using cardiotoxins

· With family history of

cardiomyopathy

Development of

symptoms of HFStructural heart

disease

6

7

Classification of Heart Failure New York Heart Association

8

Stages / Classification of Heart Failure

Sudden or gradual onset of the signs

and symptoms of heart failure requiring unplanned office visits, emergency room visits, or hospitalizations.

Associated with pulmonary and systemic congestion due to increased left and right heart filling pressures.

Rehospitalization rate predicted to be 50% at 6 months

1-year mortality of approximately 30% of ADHF admissions (ACCF/AHA 2013 HF Guidelines)

Acute Decompensated Heart Failure (ADHF)

9

Common Precipitating Factors of ADHF

Non adherence with Medications

Dietary sodium intake

Fluid intake

Acute MI

Arrhythmias Atrial fibrillation

Persistent hypertension

Recent addition of negative inotrope

Pulmonary embolism

Nonsteroidal anti-inflammatory drugs

Excessive alcohol or drug use

Endocrine abnormality

Concurrent infection

New anemia

10

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

Potential Contributing

Precipitating Factors and/or Comorbidities

11

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

Hospitalization Recommended

12

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

Hospitalization Should be Considered

13

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

Treatment Goals

14

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.

Diagnosis

15

Patient 1: Volume overload (Backwards Failure)

Patient 2: Profound depression of cardiac output –hypoperfusion (Forwards Failure)

Patient 3: Signs and symptoms of both fluid overload and hypoperfusion (cardiogenic shock)

3 Clinical Presentations

16

Determine

Volume Status

Perfusion Status

Role of / or presence of precipitating factors and/or comorbidities

Ejection fraction HFpEF

HFrEF

Evaluation Guides Treatment Decisions

17

Hypoperfusion vs. Volume Overload

18

Intravascular Volume Overload Elevated jugular

venous pressure

Hepatojugular reflex

Orthopnea

Dyspnea

Crackles

Weight gain

Peripheral edema

Hypoperfusion Narrow pulse pressure

Resting tachycardia

Cool Skin

Altered mentation

Decreased urine output

Increased BUN/Creatinine

Cheyne Stokes Respirations

0

1

4

3

2

5

20 18 16 14 12 10 8 6 4 2 32 30 28 26 24 22 34 36

Preload: PWP, lung sounds (dry or wet)

Fo

rward

s F

low

:

CI,

Sk

in t

em

p (

warm

or

cold

) Normal Hemodynamics (I) No pulmonary congestion:

• PWP < 18; Dry lungs No hypoperfusion:

• CI > 2.2; Warm skin

Backwards Failure (II) Pulmonary congestion

• PWP > 18; Wet lungs No hypoperfusion

• CI > 2.2; Warm skin

Forwards Failure (III) No pulmonary congestion

• PWP < 18; Dry lungs Hypoperfusion

• CI < 2.2; Cold skin

The Shock Box (IV) Pulmonary congestion

• PWP > 18; Wet lungs Hypoperfusion

• CI < 2.2; Cold skin

19

Hemodynamic and Clinical Subsets

20

Treatment for Acute Decompensated Heart Failure

Congestion with Adequate Perfusion

Subset II

Reduce Preload

Hypoperfusion with No Congestion

Subset III Increase contractility Assure adequate preload

Hypoperfusion with Congestion

Subset IV

Reduce Afterload 21

0

1

4

3

2

5

20 18 16 14 12 10 8 6 4 2 32 30 28 26 24 22 34 36

Preload

Fo

rwar

d F

low

: C

ard

iac

Ind

ex

S

kin

te

mp

(w

arm

or

cold

) Changing Preload: Moves patient along the current curve

22

Warm and Dry

Cold and Wet

0

1

4

3

2

5

20 18 16 14 12 10 8 6 4 2 32 30 28 26 24 22 34 36

Changing Contractility: moves patient to a higher curve

23

Preload: PWP, lung sounds (dry or wet)

Fo

rward

s F

low

:

CI,

Sk

in t

em

p (

warm

or

cold

)

0

1

4

3

2

5

20 18 16 14 12 10 8 6 4 2 32 30 28 26 24 22 34 36

Changing Afterload:: moves patient up and to the left

(improves forwards flow and reduces preload)

24

Fo

rward

s F

low

:

CI,

Sk

in t

em

p (

warm

or

cold

)

Preload: PWP, lung sounds (dry or wet)

25

Acute Decompensated Heart Failure

Reduce Afterload Arterial vasodilators High dose Nitroglycerin Nitroprusside Neseritide

Intra aortic balloon pump

Increase Contractility Positive Inotropes

Dobutamine

Milronone

Dopamine

Reduce Preload Diuretics Venous Vasodilators Low dose NTG Neseritide

Ultrafiltration

26

Pharmacological Options for Decreasing

Preload

Stop or decrease fluid

Diuretics ▪ A loop diuretic such as furosemide eliminates

circulating volume

Venous

Vasodilators

▪ Intravenous nitroglycerin, neseritide, or

morphine sulfate

(Venous vasodilatation pools blood away from

the heart and decreases preload)

ACE Inhibitors or

Angiotensin II

Receptor Blockers

(ARBs)

▪ Interrupt renin- Angiotensin- aldosterone system. (RAAS).

Aldosterone secretion is decreased and there is less sodium and

water retention.

▪ ACE inhibitors end in “pril” / ARBs end in “sartan”

Aldosterone

antagonists

▪ Spironolactone or epleranone

▪ Directly block aldosterone and there is decreased sodium and water

retention.

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

Reduce Preload Loop Diuretics

27

Diuretics and Renal Function

Role of venous congestion in worsening renal function

Role of volume depletion / hypotension and worsening renal function

28

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)

Cardiorenal Syndrome

29

30

Loop Diuretics

Bumetanide (Bumex) Equivalents Furosemide 40 mg Torsemide 20 mg Bumetanide 1 mg

Dosing

Adequate to relieve symptoms Start equal or greater than home maintenance dose

Furosemide (Lasix)

Torsemide (Demadex)

More on Loop Diuretics

31

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

Bumetanide Furosemide Torsemide

Lack of randomized control data with comparison to furosemide. Better pharmacokinetic profile (oral bioavailability) than furosemide but turosemide has evidence of more efficacy and more safety. (Wargo &Banta, 2009)

BID Dosing when GFR is low

2 randomized trials comparing Torsemide and Furosemide N=471 Torsemide associated with reduction in HF and CV readmission in systolic HF with a trend towards reduction of all cause mortality. (DiNicolantonio, 2012)

Differences in Loop Diuretics

32

Preload Reduction Venous Vasodilators

Afterload Reduction Arterial Vasodilators

Three Primary Drugs NTG

IV Primary Venous Vasodilator

Neseritide

Mixed

Nitroprusside

Predominantly Arterial Vasodilator

Vasodilator Therapy

33

Nitroglycerin

Mixed venous and arterial vasodilator Dosage < 1mcg/kg/min = venous vasodilator Dosage > 1mcg/kg/min = arterial and venous

vasodilator Sublingual tablets provide high enough dosage to

dilate arteries and veins

Caution with severe Aortic Stenosis Decreases activity of Heparin

34

Nitroglycerin

35

Uses: Acute MI, unstable angina, CHF

Side Effects:

H/A, Hypotension, flushing

Nursing Considerations: Contraindicated with

Sildenefil like drugs Caution (all venous

vasodilators) with: Hypertrophic

cardiomyopathy, aortic stenosis, right ventricular MI

Treat H/A with pain meds

and decrease dose

Onset IV: 1-2 minutes Duration: 3-5 minutes

Nesiritide (Natrecor)

Recombinant form of human B type natriuretic peptide (BNP)

BNP is a naturally occurring cardiac neurohormone secreted by the heart in the body’s response to heart failure

BNP allows the heart to participate in the regulation of vascular tone and extracellular volume status

The BNP system and the renin-angiotensin system counteract each other in heart failure

BNP levels are elevated in heart failure

36

Nesiritide (Natrecor)

Balanced arterial and venous vasodilatation Causes rapid

reduction in right and left sided ventricular filling pressures (preload reduction)

Reduces afterload

Indicated for acutely decompensated heart failure patients who have dyspnea at rest

37

Nesiritide (Natrecor)

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 24-48 hours

38

Monitor BP closely during administration.

Nesiritide: Where do we stand?

39

Balanced venous and arterial vasodilator

Sackner-Bernstein JD, Kowalski M, Fox M, Aaronson K: Short-term risk of death after treatment with nesiritide for decompensated heart failure: a pooled analysis of randomized controlled trials. JAMA 2005, 293:1900-1905.

In the 3 trials, 485 patients were randomized to nesiritide and 377 to control therapy. Death within 30 days tended to occur more often among patients randomized to nesiritide therapy (35 [7.2%] of 485 vs 15 [4.0%] of 377 patients. No statistically significant difference.

ASCEND HF Trial

40

Effect of Nesiritide in Patients with Acute Decompensated Heart Failure

O'Connor et al.

July 7 2011

7,141 patients

Randomized

Nesiritide was not associated with an increase or a decrease in the rate of death and re-hospitalization.

It was not associated with a worsening of renal function, but it was associated with an increase in rates of hypotension.

Neseritide cannot be recommended for routine use.

Nitroprusside

Mixed venous and arterial dilator (primarily arterial)

Decreases BP, SVR, PVR, PAOP, RAP

Uses: Hypertensive crisis

CHF

Acute Mitral Regurgitation

Other Indications for Afterload Reduction

Side Effects: Hypotension Thiocyanate toxicity:

tinnitus, blurred vision, delirium, seizures, muscle twitching, absent reflexes, dilated pupils [several days – high doses]

Nursing Considerations: Onset: 1-2 minutes Duration: 1-10 minutes Monitor BP carefully-

arterial line encouraged

41

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

Reduce Preload Venous Vasodilators

42

If No Improvement With Preload Reduction

Na and fluid restrict Increase dose of loop

diuretic Continuous infusion of

loop diuretic Add 2nd diuretic PO Maximize loop diuretic Metalazone Spironolactone

OR IV chlorothiazide

Consider ultrafiltration

Diuretic Resistance

Reasons

High sodium levels

NSAIDs

Severe renal impairment

Renal hypoperfusion

43

Ultrafiltration

UNLOAD Trial Veno-venus ultrafiltration

(UF) vs standard IV diuretic therapy for hypervolemic HF

200 patients randomized UF with statistical

significance for: greater weight loss (48 hours), greater fluid loss (48 hours), less 90-day resource utilization for HF.

No statistically significant difference in dyspnea scores or creatinine levels (safety endpoint)

CARESS-HF Trial Treatment of ADHF,

worsening renal function, persistent congestion with stepped pharmacologic approach vs ultrafiltration

188 patients randomized

UF: inferior to pharmacologic therapy and associated with adverse events.

44

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)

Increase Contractility Inotropes

45

46

Dobutamine

What receptors are stimulated:

Primarily β1

Some alpha1 receptor stimulation

Some β2 stimulation

Modest β2 (more β2 than alpha1)

What are the resultant actions:

Increase contractility (+ inotrope) (β1)

Increase AV node conduction

Modest vasodilation

When and why do we use: Used as an inotrope (resultant preload reduction) with modest afterload reduction

(ACC / AHA Guidelines for Heart Failure*)

What are special nursing considerations:

Onset 1 to 2 minutes; Peak 10 minutes

Half-life 2 minutes

Note: Blood pressure response is variable; β2 causes vasodilatation; β1 increases cardiac output and may increase BP

Synthetic Compound

Phosphodiesterase Inhibitors: Non Sympathomimetic Inotropes

47

Used as an

Inotrope

BUT…..

Also has……

Preload

Reduction

Afterload

Reduction

Milrinone (Primacor)

Creates + inotropic effect by increasing availability of calcium Inhibits the degradation

of cyclic AMP which is indirectly responsible for increasing the influx of calcium through the calcium channel

Smooth muscle relaxant (venous and arterial vasodilator)

Indications: Refractory heart failure

(in combination with dobutamine)

Left ventricular failure in MI

Patients waiting transplant

Side Effects: Ventricular arrhythmias,

thrombocytopenia (new generation less)

OPTIME Trial

48

OPTIME Trial Milrinone approved by FDA based on hemodynamic data Future trials need to include symptom relief and post

discharge outcome data OPTIME Prospective trial, randomized, placebo controlled 951 patients Patients had indication for but not all required inotrope for end

organ perfusion. Results: No difference in LOS, No difference in subjective

improvement Treatment failures more common in milrinone group due to

hypotension, more atrial fibrillation in milrinone Not powered for mortality differences

Conclusion: Hemodynamic improvement does not translate into clinical improvement

49

Dopamine

What receptors are stimulated:

Dopaminergic at low doses (0.5-2.0 mcg/kg/min)

β1 also at moderate doses ( 2.0-10.0 mcg/kg/min)

Pure alpha stimulation at high doses > 10mcg/kg/min

What are the resultant actions:

Increase GFR at low doses

Increase contractility at moderate doses (greater effects on contractility than heart rate)

Vasoconstriction (alpha) at high doses

When and why do we use:

Refractory hypotension / shock

* Not indicated for routine treatment or prevention of acute renal failure

What are special nursing considerations:

Onset 1-2 minutes; Peak 10 minutes

Maximal effects @20/mcg/kg/min

Large IV line or central line; Regitine (alpha blocker) for infiltrate

50

Mimics endogenous dopamine;

metabolic precursor

of norepinephrine and epinephrine

Comparison of Dopamine to Norepinephrine in Shock

51

Backer et al.

Multi Center Randomized Controlled Trial

New England Journal of Medicine

March 4th 2010

There were no significant differences between the groups in the rate of death at 28 days or in the rates of death in the ICU, in the hospital, at 6 months, or at 12 months

More patients with arrhythmia in the dopamine group

Rate of death was higher in predefined subgroup analysis for patients with cardiogenic shock treated with dopamine.

Acute Decompensated Heart Failure

52

Reduce Preload Diuretics Venous vasodilators Low dose Nitroglycerin Neseritide

Ultrafiltration

Reduce Afterload Arterial vasodilators High dose Nitroglycerin Nitroprusside Neseritide

Intra aortic balloon pump

Increase Contractility Positive Inotropes Dobutamine

Milronone

Dopamine

53

Serelaxin RELAX –AHF Trail

Presented AHA November 2012

Recombinant human relaxin-2, vasoactive peptide hormone

Double blinded placebo controlled, randomized trial

Standard care plus 48 hours of serelaxin or placebo

1161 patients

Positive outcomes:

Dyspnea relief

Improvement in signs and symptoms of HF

Reduction in LOS

Decreased all cause and CV 180 day mortality (37% reduction in mortality)

No impact on readmissions

Europe Regulators - Denied approval January 2014

Breakthrough therapy designation by FDA – June 21 2013

Pending FDA approval Feb 13, 2014.

Additional Care Issues

54

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

Invasive Monitoring

55

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

Foley Catheter

56

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

Fluid Restriction

57

Oxygen therapy is recommended if the patient exhibits hypoxemia

If not hypoxemic no need for oxygen therapy

Use of non-invasive positive pressure ventilation may be considered for severely dyspneic patients with clinical evidence of pulmonary edema.

58

Continue other evidence based practice medications

Daily monitoring of volume status via

Daily weights

Fluid balance

JVP

Orthopnea

Orthostatic pressures

Activity tolerance

Perceived dyspnea

Other considerations

59

Bridge to transplant (BBT) for those who are

transplant eligible

Destination therapy (DT) for those who are not transplant eligible.

Bridge to Decision (BTD)

Careful consideration for all therapies Some patients may be too ill with multisystem issues

to benefit from MCS

Some decisions are best made in the hands of the most experienced centers

60

Profile 1: Cardiogenic Shock Profound hypotension despite rapidly escalating inotropic

support; acidosis; “crash and burn”

Profile 2: Progressive decline Declining function despite IV inotropes, possible worsening

renal function; “sliding on inotropes”

Profile 3: Stable but inotrope-dependent Continuous IV inotropes +/- IABP or other mechanical

support, unable to be weaned

61

Profile of Severe Heart Failure

Margarita Camacho MD, FACS Surgical Director - Cardiac Transplant and Mechanical Assist Device Program Barnabas Health Heart Centers at Newark Beth Israel Medical Center, Newark, NJ

Profile 4: Resting Symptoms Daily congestion at rest or during ADL (activities of

daily living)

Profile 5: Exertion intolerant Comfortable at rest or with ADL, but unable to engage

in any other activity, living predominantly within house

Profile 6: Exertion limited Comfortable at rest and with ADL.

Profile 7: Advanced NYHA III Living comfortably with meaningful activity limited to

mild physical exertion

62

Profile of Severe Heart Failure

63

IABP

ECMO

Impella

CentriMag

Thoratec pVAD

Abiomed AB 5000

Abiomed BVS 5000

64

Temporary Assist Devices in Acute Shock

Intra Aortic Balloon Pump

65

66

Impella

Pulls blood from the left ventricle and expels blood into the ascending aorta.

Inserted via femoral artery, into the ascending aorta, across the valve and into the left ventricle.

Produces CO of 2.5 – 5.0 L/Min (2 different devices)

Impella

Mechanical Cirulatory Support Device

“Percutaneous VAD”

Minimally invasive

Unloads ventricle reducing myocardial workload

Produces 2.5 liters of cardiac output

Recommended for up to 7 days

Bridge to Recovery

67

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

Bridge to Recovery

68

69

Cardiac arrest with ongoing CPR

Cardiogenic shock, IABP-dependent on inotropes and pressors

Intra-operative failure to wean from cardiopulmonary bypass

Bridge to a decision: indeterminate neurologic status or other significant co-morbidity (i.e., possible incurable malignancy) with critical clinical deterioration

70

Who Gets a Device Acutely

CentriMag

AB5000

PVAD or IVAD

Alternate: Impella 5.0 or Tandem Heart

71

Cardiac Arrest with Ongoing CPR

CentriMag

Impella 5.0

Tandem Heart

PVAD or IVAD

72

Cardiogenic Shock, IABP Dependent on Inotropes and Pressors

CentriMAG

Tandem Heart or Impella 5.0

PVAD OR IVAD (if suspect patient will need long-term support)

AB5000 (concerns about coagulopathy/increased hemolysis after long bypass runs

73

Intra-operative failure to wean from CP Bypass

Bridge to a decision: indeterminate neurologic status

or other significant co-morbidity (i.e., possible incurable malignancy) with critical clinical deterioration

CentriMag

AB5000

Impella 5.0

Tandem Heart

74

Bridge to Decision

Thoratec pVAD

Abiomed AB 5000

Abiomed BVS 5000

Heart Mate XVE

Heart Mate II

HeartWare HVAD

Cardiowest Total Artificial Heart

75

BiV Bridge to Transplant

Long Term Therapy

BTT

Thoratec pVAD

Abiomed AB 5000

Abiomed BVS 5000

Heart Mate XVE

Heart Mate II

HeartWare HVAD

DT

Heart Mate XVE

Heart Mate II

HeartWare HVAD

76

Criteria for Discharge

Exacerbating factors addressed

Near optimal volume status achieved

Transition from intravenous to oral diuretic successfully completed

Patient and family education completed, including clear discharge instruction

LVEF documented

Smoking cessation counseling initiated

Near optimal pharmacologic therapy achieved, including ACE inhibitor and beta-blocker (for patients with reduced LVEF), or intolerance documented

Follow-up clinic visit scheduled, usually for 7 to 10 d 77

Criteria for Discharge

Advanced HF Patient or recurrent admission Oral medication regimen stable for 24 h

No intravenous vasodilator or inotropic agent for 24 h

Ambulation before discharge to assess functional capacity after therapy

Plans for post discharge management (scale present in home, visiting nurse or telephone follow up generally no longer than 3 d after discharge)

Referral for disease management, if available

78

Advanced HF

Decision Making

79

Currently 2.4% of adult population affected with HF

Over 11% of the expanding population is > 80 years

80

Things to Think About

Heart Failure Survival Score All cause mortalilty

Seattle Heart Failure Model All cause mortality, urgent transplantation or LVAD implant depts.washington.edu.shfm

EVEREST Risk Model Combined endpoint of mortality or persistently poor quality of life

over the 6 months after discharge EFFECT 30-day and 1-year mortality

ADHERE In-hospital mortality

ESCAPE Discharge Score 6 month mortality

81

Prognostic Models

>2 Prompt Referral for Advanced Rx

Hospitalization for HF on oral HF therapy

Inability to take ACEI/ARB/BB

BUN> 45, Creat>2.5, CrCl< 45 cc/min

BNP >4 x’s upper limit of normal

Na+ < 136

Malnutrition/Cachexia

VO2 <55% predicted

LVEDD >7.0 cm

82

Risk Factors for Mortality > 2 Referral for Advanced Treatment

83

Moderate to severe symptoms of dyspnea and/or fatigue at rest or with minimal exertion (NYHA functional class III or IV)

Episodes of fluid retention and/or reduced cardiac output

Objective evidence of severe cardiac dysfunction demonstrated by at least 1 of the following: Left ventricular ejection fraction <30%

Pseudonormal or restrictive mitral inflow pattern by Doppler

High left and /or right ventricular filling pressures, or

Elevated B-type natriuretic peptide

Severe impairment of functional capacity as demonstrated by either inability to exercise, 6-min walk distance 300 m, or peak oxygen uptake <12 to 14 mL g-1 min-1

History of at least 1 hospitalization in the past 6 months

Characteristics should be present despite optimal medical therapy

European Society of Cardiology Criteria for Advanced Chronic Heart Failure

84

85

Palliative Care versus Hospice

When should they be involved

Making an assessment

Having the discussion

86

End of Life Decision

+20% to -

68%

P=0.1566

-43% to -91%

P<0.0001

-70% to -96%

P<0.0001

Fonarow GC,Yancy CW. J Am Heart Assoc 2012;1:16-26.

87

Number of Therapies (vs 0 or 1 therapy)

2 therapies

3 therapies

4 therapies

5, 6, or 7 therapies

Odds Ratio (95% confidence interval)

0.63 (0.47-0.85) (p=0.0026)

0.38 (0.29-0.51) (p<0.0001)

0.30 (0.23-0.41) (p<0.0001)

0.31 (0.23-0.42) (p<0.0001)

0 0.5 1 1.5 2

Fonarow GC, … Yancy, C. J Am Heart Assoc 2012;1:16-26. 88

89

We must not, in trying to think about how we can make a big difference, ignore the small daily differences we can make which, overtime, add up to big differences that we often cannot foresee.

-Marian Wright Edelman

A Final Thought:

90

BE THE BEST THAT YOU CAN BE

EVERY DAY. YOUR PATIENTS ARE

COUNTING ON IT!