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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
2014
www.cardionursing.com
2

They may forget your
name, but they will never
forget how you made
them feel.
-Maya Angelou
3
Definitions

4
Definition of Heart Failure
Classification
Ejection
Fraction
I. Heart Failure with
Reduced Ejection
Fraction (HFrEF)
≤40%
II. Heart Failure
with Preserved
Ejection Fraction
(HFpEF)
≥50%
a. HFpEF,
Borderline
41% - 49%
b. HFpEF
Improved
>40%
Description
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.
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.
These patients fall into a borderline or intermediate group. Their
characteristics, treatment patterns, and outcomes appear similar to
those of patient with HFpEF.
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
5
to better characterize these patients.
Stages, Phenotypes and Treatment of HF
At Risk for Heart Failure
Heart Failure
STAGE A
STAGE B
STAGE C
At high risk for HF but
without structural heart
disease or symptoms of HF
Structural heart disease
but without signs or
symptoms of HF
Structural heart disease
with prior or current
symptoms of HF
e.g., Patients with:
· HTN
· Atherosclerotic disease
· DM
· Obesity
· Metabolic syndrome
or
Patients
· Using cardiotoxins
· With family history of
cardiomyopathy
Structural heart
disease
e.g., Patients with:
· Previous MI
· LV remodeling including
LVH and low EF
· Asymptomatic valvular
disease
Development of
symptoms of HF
e.g., Patients with:
· Known structural heart disease and
· HF signs and symptoms
HFpEF
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
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
STAGE D
Refractory 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
Refractory
symptoms of HF
at rest, despite
GDMT
e.g., Patients with:
· Marked HF symptoms at
rest
· Recurrent hospitalizations
despite GDMT
HFrEF
THERAPY
Goals
· 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
THERAPY
Goals
· Control symptoms
· Improve HRQOL
· Reduce hospital
readmissions
· Establish patient’s endof-life goals
Options
· Advanced care
measures
· Heart transplant
· Chronic inotropes
· Temporary or permanent
MCS
· Experimental surgery or
drugs
· Palliative care and
hospice
· ICD deactivation
6
Classification of Heart Failure
New York Heart Association
7
Stages / Classification of Heart Failure
8
Acute Decompensated
Heart Failure (ADHF)

 Sudden or gradual onset of the signs
and symptoms of heart failure
requiring unplanned office visits,
emergency room visits, or
hospitalizations.
 Associated with pulmonary and
systemic congestion due to
increased left and right heart filling
pressures.
 Rehospitalization rate predicted to
be 50% at 6 months
 1-year mortality of approximately
30% of ADHF admissions
(ACCF/AHA 2013 HF Guidelines)
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 antiinflammatory drugs
 Excessive alcohol or
drug use
 Endocrine abnormality
 Concurrent infection
 New anemia
10
Potential Contributing
Precipitating Factors and/or Comorbidities

 ACS / coronary ischemia (troponins typically elevated
with ADHF)
 Severe hypertension
 Atrial or ventricular arrhythmias
 Infections
 Pulmonary emboli
 Renal failure
 Medical or dietary compliance
 Valvular heart disease
 New onset anemia
11
Hospitalization
Recommended

Evidence of severe ADHF, including:
 Hypotension
 Worsening renal function
 Altered mentation
Dyspnea at rest
 Typically reflected by resting tachypnea
 Less commonly reflected by oxygen saturation <90%
Hemodynamically significant arrhythmia - including
new onset of rapid atrial fibrillation
Acute coronary syndromes
12
Hospitalization
Should be Considered

Worsened congestion: Even without dyspnea
Signs and symptoms of pulmonary or systemic congestion
 Even in the absence of weight gain
Major electrolyte disturbance
Associated comorbid conditions
 Pneumonia
 Pulmonary embolus
 Diabetic ketoacidosis
 Symptoms suggestive of transient ischemic accident or
stroke
Repeated ICD firings
Previously undiagnosed HF with signs and symptoms of
systemic or pulmonary congestion
13











Treatment Goals

Improve symptoms, especially congestion and low-output symptoms
Optimize volume status
Identify etiology
Identify and address precipitating factors
Optimize chronic oral therapy
Minimize side effects
Identify patients who might benefit from revascularization
Identify patients who might benefit from device therapy
Identify risk of thromboembolism and need for anticoagulant therapy
Educate patients concerning medications and self management of HF
Consider and, where possible, initiate a disease management
14
program
Diagnosis

Based on signs and symptoms
B-type natriuretic peptide (BNP) or N-terminal
pro-B-type natriuretic peptide (NT-proBNP)
 Good to assess in patients with dyspnea being evaluated
for HF
 Should not be used as the sole tool to diagnose HF
 Must be used in concert with signs and symptoms
 Special consideration with renal insufficiency and
obesity.
15
3 Clinical Presentations

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)
16
Evaluation Guides
Treatment Decisions

Determine
Volume Status
Perfusion Status
Role of / or presence of precipitating
factors and/or comorbidities
Ejection fraction
HFpEF
HFrEF
17
Hypoperfusion vs. Volume
Overload
Hypoperfusion

 Narrow pulse pressure
 Resting tachycardia
 Cool Skin
 Altered mentation
 Decreased urine output
 Increased
BUN/Creatinine
 Cheyne Stokes
Respirations
Intravascular
Volume Overload
 Elevated jugular
venous pressure






Hepatojugular reflex
Orthopnea
Dyspnea
Crackles
Weight gain
Peripheral edema
18
Hemodynamic and Clinical Subsets
Forwards Flow:
CI, Skin temp (warm or cold)
5
Normal Hemodynamics (I)
Backwards Failure (II)
3
No pulmonary congestion:
• PWP < 18; Dry lungs
No hypoperfusion:
• CI > 2.2; Warm skin
Pulmonary congestion
• PWP > 18; Wet lungs
No hypoperfusion
• CI > 2.2; Warm skin
2
Forwards Failure (III)
1
No pulmonary congestion
• PWP < 18; Dry lungs
Hypoperfusion
• CI < 2.2; Cold skin
4
The Shock Box (IV)
Pulmonary congestion
• PWP > 18; Wet lungs
Hypoperfusion
• CI < 2.2; Cold skin
0
2
4
6
8
10 12 14 16 18 20 22 24 26 28 30 32 34 36
Preload: PWP, lung sounds (dry or wet)
19
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
Changing Preload: Moves patient along the current curve
Forward Flow: Cardiac Index
Skin temp (warm or cold)
5
Warm and
Dry
4
3
2
1
Cold and
Wet
0
2
4
6
8
10 12 14 16 18 20 22 24 26 28 30 32 34 36
Preload
22
Changing Contractility: moves patient to a higher
Forwards Flow:
CI, Skin temp (warm or cold)
curve
5
4
3
2
1
0
2
4
6
8
10 12 14 16 18 20 22 24 26 28 30 32 34 36
Preload: PWP, lung sounds (dry or wet)
23
Changing Afterload:: moves patient up and to the left
Forwards Flow:
CI, Skin temp (warm or cold)
(improves forwards flow and reduces preload)
5
4
3
2
1
0
2
4
6
8
10 12 14 16 18 20 22 24 26 28 30 32 34 36
Preload: PWP, lung sounds (dry or wet)
24
Acute Decompensated
Heart Failure
Reduce Preload
 Diuretics
 Venous Vasodilators
 Low dose NTG
 Neseritide
 Ultrafiltration
Increase Contractility
 Positive Inotropes
 Dobutamine
 Milronone
 Dopamine
 Reduce Afterload
 Arterial vasodilators
 High dose Nitroglycerin
 Nitroprusside
 Neseritide
 Intra aortic balloon
pump
25
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.
26
Reduce Preload
Loop Diuretics

 IV not PO
 Early intervention - ED
 Dose high enough to relieve signs and symptoms of
congestion
 Should equal or exceed chronic oral dose
 Caution for signs of over diuresis
 Hypotension: check orthostatics
 Worsening renal failure
 Monitor e-lytes (potassium, magnesium, sodium)
 Arrhythmias
 Muscle cramps
 Monitor for gout
 Frequent reassessment
27
Diuretics and Renal
Function

 Role of venous congestion in worsening renal
function
 Role of volume depletion / hypotension and
worsening renal function
28
Cardiorenal Syndrome

Moderate to severe renal dysfunction with fluid
overload
 Continue to treat with diuretics
In severe fluid overload renal dysfunction my
improve with continued treatment
 May need to hold ACE I secondary to AKI
 Venous congestion plays a role in worsening renal
function (not just hypoperfusion)
29
Loop Diuretics
Bumetanide (Bumex)
Furosemide (Lasix)
Torsemide (Demadex)
Equivalents
Furosemide 40 mg
Torsemide 20 mg
Bumetanide 1 mg
Dosing
Adequate to relieve symptoms
Start equal or greater than home
maintenance dose
30
More on Loop Diuretics

DOSE Trial
 NEJM: Felker et al., 2011
 No significant difference in symptoms or renal
function between continuous drip versus
intermittent dosing
 Non significant trend toward improvement in
symptoms with high dose (IV at 2.5 x PO dose)
versus low dose; (IV at same as PO dose) no change in
31
renal function
Differences in Loop
Diuretics
Furosemide
Bumetanide
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)
32
Vasodilator Therapy

 Preload Reduction
 Venous Vasodilators
 Afterload Reduction
 Arterial Vasodilators
 Three Primary Drugs
 NTG
 IV Primary Venous Vasodilator
 Neseritide
 Mixed
 Nitroprusside
 Predominantly Arterial Vasodilator
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
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
35
Nesiritide (Natrecor)
 Recombinant form of
human B type
natriuretic peptide
(BNP)
 BNP allows the heart to
 BNP is a naturally
occurring cardiac
neurohormone secreted
by the heart in the
body’s response to
heart failure
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)

 Given by IV bolus
Patient must have
systolic BP > 90
mmHg
and maintenance
infusion (bolus to be
taken from
reconstituted IV bag
and not from vial)
PAOP should be
estimated to be > 20
 Infusion is usually 24mmHg
48 hours
Monitor BP closely during administration.
38
Nesiritide: Where do we stand?

 Balanced venous and arterial vasodilator
 Sackner-Bernstein JD, Kowalski M, Fox M, Aaronson K:
Short-term risk of death after treatment with nesiritide
for decompensated heart failure: a pooled analysis of
randomized controlled trials. JAMA 2005, 293:1900-1905.
 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
39
difference.
ASCEND HF Trial

 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.
40
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 carefullyarterial line encouraged
41
Reduce Preload
Venous Vasodilators

Persistent failure with aggressive diuresis
and standard oral therapies
 NTG
 Neseritide
 Nitroprusside
 Especially helpful with severe hypertension or severe
MR
 For rapid symptom relief in acute pulmonary edema
with hypertension
 NTG / Nitroprusside
 Do not give with hypotension
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
Diuretic Resistance
Reasons
 High sodium levels
 NSAIDs
 Severe renal
impairment
 Renal hypoperfusion
 OR IV chlorothiazide
 Consider ultrafiltration
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
Increase Contractility
Inotropes

 Goal: Relief of symptoms and end organ perfusion
 Use in:
 Low output states
 Symptomatic hypotension or marginal blood pressure
 Despite good filling pressures
 No magic blood pressure – look for symptoms
 Unresponsive / intolerant of IV vasodilators
 Diminished or worsening renal function
 Use vasodilators first as able
 Monitor closely for tachyarrhythmias and hypotension
 Not recommended if normotensive (ACC)
45
Synthetic Compound
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 output46
and may increase BP
Phosphodiesterase Inhibitors: Non
Sympathomimetic Inotropes

Used as an
Inotrope
Preload
Reduction
Also has……
BUT…..
Afterload
Reduction
47
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:
Mimics endogenous dopamine;
metabolic precursor
of norepinephrine and epinephrine
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 Increase GFR at low doses
actions:
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
Comparison of Dopamine to Norepinephrine in Shock
 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.
51
Acute Decompensated
Heart Failure
Reduce Preload
 Diuretics
 Venous vasodilators
 Low dose Nitroglycerin
 Neseritide
Increase
Contractility
 Positive Inotropes
 Dobutamine
 Milronone
 Dopamine
52
 Ultrafiltration
Reduce Afterload
 Arterial vasodilators
 High dose Nitroglycerin
 Nitroprusside
 Neseritide
 Intra aortic balloon
pump











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
53
Pending FDA approval Feb 13, 2014.
Additional Care Issues

54
Invasive Monitoring

Routine use not recommended
When to consider:
 Refractory to initial therapy
 Volume status and cardiac filling pressures are
unclear
 Pulmonary and systemic pressures unclear
 Clinically significant hypotension (SBP < 80 mm
Hg)
 Worsening renal function
55
Foley Catheter

Foley Catheter
Not recommended routinely in heart
failure
If need to closely monitor hourly urine
output
Possible outlet obstruction
 High risk patients include those with BPH
and or right sided volume overload
56
Fluid Restriction

 Dietary Sodium Restriction
 Water follows sodium
 If hyponatremic
 Serum sodium < 130 mEq/L
 2 liters per day
 Serum Sodium < 125 mEq/L
 Stricter fluid restriction may be considered
 If persistent fluid overload
 Assure sodium restriction in conjunction with fluid
restriction
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
Other considerations

 Continue other evidence based practice medications
 Daily monitoring of volume status via







Daily weights
Fluid balance
JVP
Orthopnea
Orthostatic pressures
Activity tolerance
Perceived dyspnea
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 of Severe Heart Failure

 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
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
61
Profile of Severe Heart Failure

 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
63
Temporary Assist Devices
in Acute Shock

 IABP
 ECMO
 Impella
 CentriMag
 Thoratec pVAD
 Abiomed AB 5000
 Abiomed BVS 5000
64
Intra Aortic Balloon Pump
65
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)
66
Bridge to Recovery

 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
67
Bridge to Recovery

 ECMO
 Extracorporeal Membrane Oxygenation
 Used to treat medically refractory cardiogenic shock
with poor oxygenation
 Provides biventricular support
 Not good for long term durability
 Used in a short term situation
 Requires perfusion support
68
69
Who Gets a Device Acutely

 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
Cardiac Arrest with Ongoing CPR

 CentriMag
 AB5000
 PVAD or IVAD
 Alternate: Impella 5.0 or Tandem Heart
71
Cardiogenic Shock, IABP Dependent
on Inotropes and Pressors

 CentriMag
 Impella 5.0
 Tandem Heart
 PVAD or IVAD
72
Intra-operative failure to wean
from CP Bypass

 CentriMAG
 Tandem Heart or Impella 5.0
 PVAD OR IVAD (if suspect patient will need longterm support)
 AB5000 (concerns about coagulopathy/increased
hemolysis after long bypass runs
73
Bridge to Decision

 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
BiV Bridge to Transplant

 Thoratec pVAD
 Abiomed AB 5000
 Abiomed BVS 5000
 Heart Mate XVE
 Heart Mate II
 HeartWare HVAD
 Cardiowest Total Artificial Heart
75
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
77
 Follow-up clinic visit scheduled, usually for 7 to 10 d
Criteria for Discharge

Advanced HF Patient or recurrent
admission
 Oral medication regimen stable for 24 h
 No intravenous vasodilator or inotropic agent for 24 h
 Ambulation before discharge to assess functional capacity
after therapy
 Plans for post discharge management (scale present in
home, visiting nurse or telephone follow up generally no
longer than 3 d after discharge)
 Referral for disease management, if available
78
Advanced HF

Decision Making
79
Things to Think About

 Currently 2.4% of adult population affected with HF
 Over 11% of the expanding population is > 80 years
80
Prognostic Models

 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
Risk Factors for Mortality
> 2 Referral for Advanced Treatment

 >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
European Society of Cardiology Criteria for
Advanced Chronic Heart Failure
 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
83
 Characteristics should be present despite optimal medical therapy
84
85
End of Life Decision

 Palliative Care versus Hospice
 When should they be involved
 Making an assessment
 Having the discussion
86
+20% to 68%
P=0.1566
-43% to -91%
P<0.0001
-70% to -96%
P<0.0001
87
Fonarow GC,Yancy CW. J Am Heart Assoc 2012;1:16-26.
Number of Therapies
(vs 0 or 1 therapy)
Odds Ratio
(95% confidence interval)
2 therapies
0.63 (0.47-0.85)
(p=0.0026)
3 therapies
0.38 (0.29-0.51)
(p<0.0001)
4 therapies
0.30 (0.23-0.41)
(p<0.0001)
5, 6, or 7 therapies
0.31 (0.23-0.42)
(p<0.0001)
0
0.5
1
1.5
Fonarow GC, … Yancy, C. J Am Heart Assoc 2012;1:16-26.
2
88
A Final Thought:
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
89
BE THE BEST THAT YOU CAN BE
EVERY DAY. YOUR PATIENTS ARE
COUNTING ON IT!
90