“I’m not telling you it is going to be easy, I’m telling you it is going …€¦ · · 2015-02-16 1 Cynthia Webner DNP, RN, CCNS, CCRN-CMC, CHFN Karen Marzlin DNP, RN, CCNS,

www.cardionursing.com 1

Cynthia Webner DNP, RN, CCNS, CCRN-CMC, CHFN Karen Marzlin DNP, RN, CCNS, CCRN-CMC, CHFN Handouts at www.cardionursing.com

2

“I’m not telling you it

is going to be easy, I’m

telling you it is going

to be worth it.”

~ Art Williams


Definition

• Heart Failure is a complex clinical syndrome resulting from any structural or functional cardiac disorder impairing the ability of the ventricle to either fill or eject

Clinical Syndrome Resulting Clinical Manifestations

Dyspnea and fatigue May limit exercise

tolerance

Fluid overload

May lead to pulmonary

congestion and peripheral edema

AND / OR

Impaired functional capacity and quality of life


Definitions

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.


HFrEF (Systolic Dysfunction) vs HFpEF (DiastolicDysfunction)

HFrEF - Systolic Dysfunction

• Impaired wall motion and ejection

• Dilated chamber

• 50% of HF Population

• Hallmark: Decreased LV Ejection Fraction < 40%

• Coronary artery disease is cause in 2/3 of patients

• Remainder – other causes of LV dysfunction

Cardiomyopathy not synonymous with HF


• Filling impairment • Normal chamber size • 50% of patients with HF have

preserved LV function • Normal EF or elevated • Caused by Hypertension Restrictive myopathy (C) Ischemic heart disease Ventricular hypertrophy (D) Valve disease Idiopathic

HFpEF - Diastolic Dysfunction

Primarily disease of elderly women with HTN

• Diagnosis is made when rate of ventricular filling is

slow

• Elevated left ventricular filling pressures when volume and contractility are normal

In practice: the diagnosis is made when

a patient has typical signs and symptoms of heart failure and has a normal or elevated

ejection fraction with no valve disease.

HFpEF - Diastolic Dysfunction


Left versus Right Sided Heart Failure

Two sides of the heart form a circuit, neither side can pump significantly more blood than the other for long

Signs/symptoms of failure reflect each respective ventricle

The Real Culprit: Neurohormonal Response

SNS Response

RAAS Response

Ventricular Remodeling


Activation of SNS

First Responder Decreased CO → ↓ BP → activates baroreceptors and vasomotor

regulatory centers in medulla

Increase circulating catecholamines Stimulates alpha and beta receptors

Increase HR

Peripheral vasoconstriction

Contractility Positive effect: ↑ CO and BP

Negative effect: ↑ O2 demand → ischemia, arrhythmias, sudden death

Chronic Stimulation of SNS

Norepinephrine (circulating catecholamine) is Cardiotoxic Decreases heart’s ability to respond to sympathetic

stimulation

Down regulation of B1 receptor sites (less sensitive)

Contributes to decreased exercise tolerance

Can also lead to ventricular remodeling

Be aware of your patient’s heart rate response to activity.


Activation of RAAS Kidney’s response to decreased perfusion due to

decreasing CO

Concentrations of angiotensin II, and aldosterone rise as end result

Potent vasoconstriction

Sodium/water absorption increases

Result

Increased preload and increased afterload

Increased myocardial oxygen demand


Harmful Result of RAAS Activation

Enhanced preload increases end-diastolic volume dilating the LV

LV becomes overstretched

LV changes size and shape (ventricular remodeling)

Contractility decreases

Congestive symptoms develop

Ventricular Remodeling

• Process of pathological growth

• Can occur from prolonged activation of SNS/RAAS

• Involves Hypertrophy of myocytes Pressure – thicken (concentric)

Volume – elongate (eccentric)

Genetically abnormal – inefficient contraction

Increased ventricular muscle mass, change in ventricular shape

Collagen matrix becomes fibrotic


Symptoms

Fluid Accumulates in Pulmonary Capillary Bed

Increased Pulmonary Pressure / Volume

Atrial Overload

Atrial Dilatation

Increased Atrial Pressure / Volume

Increased Ventricular Pressure / Volume

Decreased Ejection of Ventricular Contents

Decreased Ventricular Contractility

Ventricular Dilatation

Changes in Systolic Dysfunction

Mitral Regurgitation

Dilated Mitral Valve Annulus

Vasoconstriction / Fluid Retention

Activation of Neuro- hormonal Responses


The Good Guys: Natriuretic Peptides

Cardiac hormones secreted by myocytes Atrial natriuretic peptide (ANP) Produced in atria

Brain natriuretic peptide (BNP) Produced in ventricles in response to increased

ventricular pressure/stretching Stronger release than ANP

Promote vasodilatation (preload/afterload reduction)

Reduce sodium/water retention (diuretic response)

Reduce production/action of vasoconstrictor peptides

Plasma concentrations elevated in patients in fluid overload

Neseritide (Natrecor) is the synthetic form of BNP

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.

Low values have strong negative predictive value

Adds to prognostic information

Natriuretic Peptides

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2014 23

Causes of Elevated Naturetic Peptide Levels

Cardiac

Heart failure, including RV syndromes

Acute coronary syndrome

Heart muscle disease, including LVH

Valvular heart disease

Pericardial disease

Atrial fibrillation

Myocarditis

Cardiac surgery

Noncardiac Advancing age Anemia Renal failure Pulmonary: obstructive sleep

apnea, severe pneumonia, pulmonary

hypertension Critical illness Bacterial sepsis Severe burns Toxic-metabolic insults,

including cancer chemotherapy and envenomation

Heart Failure Symptoms

Exercise intolerance (hallmark) Ability to perform ADLs

Fatigue

Dyspnea

Paroxysmal nocturnal dyspnea

Frequent night urination with less during the day

Peripheral edema/weight change

Chest pain

GI problems

Confusion/altered mental status


Heart Failure Symptoms

Symptoms in the elderly

Many don’t experience exertional dyspnea because they are sedentary

More common:

Daytime oliguria/nocturia

Mental disturbances

Anorexia

GI disturbances

Classification of Heart Failure New York Heart Association


Physical Exam Findings General Appearance (resting dyspnea, cyanosis, cachexia)

Weight gain

BP/HR

Include orthostatic pressures

JVD

Hepatojugular reflux

Edema

Displaced apical impulse

S3/S4

Lung sounds



Treatment Strategies

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


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


· Marked HF symptoms at

rest

· Recurrent hospitalizations

despite GDMT


· Previous MI

· LV remodeling including

LVH and low EF

· Asymptomatic valvular

disease


· HTN

· Atherosclerotic disease

· DM

· Obesity

· Metabolic syndrome

or

Patients

· Using cardiotoxins

· With family history of

cardiomyopathy

Development of

symptoms of HFStructural heart

disease


HFpEF

No evidence based medical therapy

ARBs, aldosterone antagonists, and sildenafil have all been tested

ARBs and aldosterone antagonists may reduce hospitalizations but not mortality

Focus on co-morbid conditions:

HTN

Sleep apnea

Atrial Fibrillation

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


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


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


· 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


· Marked HF symptoms at

rest

· Recurrent hospitalizations

despite GDMT


· Previous MI

· LV remodeling including

LVH and low EF

· Asymptomatic valvular

disease


· HTN

· Atherosclerotic disease

· DM

· Obesity

· Metabolic syndrome

or

Patients

· Using cardiotoxins

· With family history of

cardiomyopathy

Development of

symptoms of HFStructural heart

disease


Details for HF pharmacology were

discussed during yesterday’s CV

pharmacology session.

Cardiac Resynchronization Therapy


Cardiac Resynchronization Therapy (CRT)

Treatment modality for heart failure not just pacing

Treatment modality in conjunction with drug therapy

Goals: Improve hemodynamics by restoring synchrony of

ventricular contraction

Improve quality of life

Decrease mortality and morbidity

CRT

Goal: Force biventricular pacing

Goal: Ventricular Pacing 90% of time or greater

Causes of Loss of Bi V pacing: Long AV Delays

Prolonged PVARP

ST with 1 degree AV Block

Lead dislodgement


Normal Ventricular Depolarization

Ventricular Depolarization with LBBB


Indications for CRT Therapy Patient with cardiomyopathy on GDMT for >3 mo or on GDMT and >40 d after MI, or

with implantation of pacing or defibrillation device for special indications

LVEF <35%

Evaluate general health status

Comorbidities and/or frailty

limit survival with good

functional capacity to <1 y

Continue GDMT without

implanted device

Acceptable noncardiac health

Evaluate NYHA clinical status

NYHA class I

· LVEF ≤30%

· QRS ≥150 ms

· LBBB pattern

· Ischemic

cardiomyopathy

· QRS ≤150 ms

· Non-LBBB pattern

NYHA class II

· LVEF ≤35%

· QRS 120-149 ms

· LBBB pattern

· Sinus rhythm

· QRS ≤150 ms

· Non-LBBB pattern

· LVEF ≤35%

· QRS ≥150 ms

· LBBB pattern

· Sinus rhythm

· LVEF ≤35%

· QRS ≥150 ms

· Non-LBBB pattern

· Sinus rhythm

Colors correspond to the class of recommendations in the ACCF/AHA Table 1.

Benefit for NYHA class I and II patients has only been shown in CRT-D trials, and while patients may not experience immediate symptomatic benefit, late remodeling may be avoided along

with long-term HF consequences. There are no trials that support CRT-pacing (without ICD) in NYHA class I and II patients. Thus, it is anticipated these patients would receive CRT-D

unless clinical reasons or personal wishes make CRT-pacing more appropriate. In patients who are NYHA class III and ambulatory class IV, CRT-D may be chosen but clinical reasons and

personal wishes may make CRT-pacing appropriate to improve symptoms and quality of life when an ICD is not expected to produce meaningful benefit in survival.

NYHA class III &

Ambulatory class IV

· LVEF ≤35%

· QRS 120-149 ms

· LBBB pattern

· Sinus rhythm

· LVEF ≤35%

· QRS 120-149 ms

· Non-LBBB pattern

· Sinus rhythm

· LVEF ≤35%

· QRS ≥150 ms

· LBBB pattern

· Sinus rhythm

· LVEF≤35%

· QRS ≥150 ms

· Non-LBBB pattern

· Sinus rhythm

· Anticipated to require

frequent ventricular

pacing (>40%)

· Atrial fibrillation, if

ventricular pacing is

required and rate

control will result in

near 100%

ventricular pacing

with CRT

Special CRT

Indications

Internal Monitoring with CRT

Heart rate variability

Patient activity

Night heart rate

Impedance

Routine re-evaluation of pacing burden is important in the treatment of HF. If HF

worsens assess CRT function.


Automatic Implantable Cardioverter Defibrillators


ICD Device

Pulse Generator Single chamber, dual chamber, or biventricular pacing

Back up pacing

Antitachycardia pacing

Implanted subcutaneously – same as pacemaker

Defibrillator lead Detects arrhythmias

Delivers therapy

Defibrillator lead capable of pacing and defibrillating

Placed in right ventricle

ICD Functions

ATP-Anti tachycardia Pacing Tiered Antiarrhythmic Therapies

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ICD Functions

Cardioversion Shock Delivers shocks from 0.1 to 30 joules synchronized on the

R wave

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ICD Functions

Defibrillating Shock Delivers high energy (20-34 joules) unsynchronized shock

for VF


Acute Decompensated Heart Failure

47

Common Precipitating Factors of ADHF

Non adherence with

Medications

Dietary sodium intake

Fluid intake

Excessive alcohol or drug use

ACS

Arrhythmias

Persistent hypertension

Valvular heart disease

Recent addition of negative inotrope

Nonsteroidal anti-inflammatory drugs

Worsening renal function

Endocrine abnormality

Concurrent infection

New anemia

Pulmonary embolism


Evidence of severe ADHF, including:

Hypotension


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

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


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

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


Determine

Volume Status

Perfusion Status

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

Ejection fraction HFpEF

HFrEF

Evaluation Guides Treatment Decisions

Hypoperfusion vs. Volume Overload

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: Pulmonary artery occlusive

pressure

Fo

rwa

rds

Flo

w:

CI,

Sk

in t

em

p (

wa

rm o

r c

old

)

Normal Hemodynamics (I) No pulmonary congestion:

• PAOP < 18; Dry lungs

No hypoperfusion:

• CI > 2.2; Warm skin

Backwards Failure (II) Pulmonary congestion

• PAOP > 18; Wet lungs

No hypoperfusion

• CI > 2.2; Warm skin

Forwards Failure (III) No pulmonary congestion

• PAOP < 18; Dry lungs

Hypoperfusion

• CI < 2.2; Cold skin

The Shock Box (IV) Pulmonary congestion

• PAOP > 18; Wet lungs

Hypoperfusion

• CI < 2.2; Cold skin

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Hemodynamic and Clinical Subsets

2014

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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

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

Forw

ard

s Fl

ow

: C

ard

iac

Ind

ex

Skin

te

mp

(w

arm

or

cold

)

Preload changes: move patient along the current curve

58


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

Preload

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)

Fo

rward

s F

low

:

CI,

Sk

in t

em

p (

warm

or

cold

)

Preload


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

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.


Additional Care Issues

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)



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

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


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.

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


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

Advanced HF

Decision Making


Severe symptoms of HF with dyspnea and/or fatigue at rest

or with minimal exertion (NYHA class IIIb or IV) on optimal medical therapy

Repeated episodes of fluid retention (pulmonary and/or systemic congestion, peripheral edema) and/or reduced cardiac output at rest (peripheral hypoperfusion) on optimal medical therapy

Objective evidence of severe cardiac dysfunction shown by at least 1 of the following on optimal medical therapy: LVEF <30% Mean PCWP >16 mmHg and/or RAP >12 mmHg by PA

catheterization High BNP or NT-proBNP plasma levels in the absence of

non-cardiac causes

Indicators for Advanced Heart Failure

Severe impairment of functional capacity while on optimal medical therapy shown by 1

of the following:

Inability to exercise

6-Minute walk distance < 300 m

Peak Vo2 <12 to 14 mL/kg/min

Repeated (≥2) hospitalizations or ED visits for HF in the past year or > 1 hospitalization for heart failure

Progressive deterioration in renal function

Progressive decline in serum sodium, usually to <133 mEq/L

Weight loss without other cause

Intolerance to ACE inhibitors due to hypotension and/or worsening renal function

Intolerance to beta blockers due to worsening HF or hypotension

Frequent systolic blood pressure <90 mm Hg

High diuretic requirements to maintain volume status (i.e. furosemide equivalent dose >160 mg/d and/or use of supplemental metolazone therapy)

Frequent ICD shocks

Indicators for Advanced Heart Failure


Heart Failure Survival Score All cause mortality

Seattle Heart Failure Model All cause mortality, urgent transplantation or LVAD implant

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

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

Risk Factors for Mortality > 2 Referral for Advanced Treatment



Palliative Care versus Hospice

When should they be involved

Making an assessment

Having the discussion

End of Life Decision Making

Establishing trust

Identifying patient values, preferences, and goals for care early in the course of treatment

Using the framework “Ask-Tell-Ask” to determine both what patients know and what they want to know

Understanding the reasons why there are conflicts regarding decisions of care

Using numeric data in a clear and understandable way as a decision aid

Respecting that patient’s may change their goals as the disease progresses

Components of effective shared decision making include:

Allen, 2012.


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

Absolute and Relative Contraindications for Durable MCS

Absolute Contraindications

Relative Contraindications

· Irreversible hepatic disease

· Irreversible renal disease · Irreversible neurological

disease · Major coagulopathy · Right sided heart failure

(unless candidate for biventricular support)

· Medical non-adherence · Severe psychosocial

limitations

· * Hypertrophic, infiltrative, or restrictive cardiomyopathy

· Uncorrectable moderate or greater aortic insufficiency

· Age _80 y(for destination therapy) · Obesity or malnutrition · MS disease that impairs rehabilitation · Active systemic infection · Prolonged intubation · Untreated malignancy · Severe PVD · Active substance abuse · Impaired cognitive function · Unmanaged psychiatric disorder · Lack of social support

Source: Peura et al., 2012; Slaughter et al., 2010. * May be a relative contraindication


Temporary Assist Devices in Acute Shock / Bridge to Decision or

Recovery

IABP

ECMO

Percutaneously implanted MCS

Impella

Tandem Heart

Surgically implanted extracorporeal MCS

CentriMag

Thoratec pVAD II

Abiomed BVS 5000

Abiomed AB 5000

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Cardiac arrest with ongoing CPR

Cardiogenic shock, IABP-dependent on inotropes and vasopressors

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

Who Gets a Device Acutely


Long Term Therapy

Bridge to Transplant

Extracorporeal MCS Thoratec pVAD II

Implantable MCS Heart Mate II

HeartWare HVAD

Total Artificial Heart CardioWest

Abiomed: Abiocor II

Destination Therapy

Heart Mate II

HeartWare HVAD

Investigational Devices

Heart Mate II

2014 86


HeartWare HVAD

2014 87

EDUCATION

EDUCATION

EDUCATION


I sure hope my wife is

getting this?

Are we going to be able to afford these

medications?

BLAH, BLAH, BLAH, BLAH!

ANY QUESTIONS? No, I think

we’ve got it.

Discharge Focus 1. Diet and Nutrition

2. Discharge Medications

3. Activity Level

4. Follow up appointments

5. Daily Weight

6. Response to symptoms


ACC / AHA Guidelines

“the addition of a 1-hour, nurse educator– delivered teaching session

at the time of hospital discharge using standardized instructions

resulted in improved clinical outcomes, increased self-care

measure adherence, and reduced cost of care”

Education and Counseling • Individualized education and counseling to focus on self care

• Should be delivered by providers using a team approach in which nurses with expertise in HF management provide the majority of education and counseling (HFSA 2010).

• Patients’ literacy, cognitive status, psychological state, culture, and access to social and financial resources should be taken into account for optimal education and counseling.

• Treat depression and anxiety to improve education comprehension

• Repeat, repeat, repeat

• Use “teach back” method

• Hospital education should be limited to “essential” education


Who should be involved?

93

Identify primary care giver / support person

and include in ALL education.

The Best Treatment Patient Education & Self-Care Maintenance and Self-Care Management

• Self-care maintenance following the rules and instructions related to the

disease process

• Self-care management decision-making process and critical thinking to make

decisions in response to changes in the client’s current health status


Self-Care Behaviors

Rationale for self-care behaviors: smoking cessation; daily weight monitoring; avoidance of heavy alcohol intake; avoidance of nonsteroidal antiinflammatory drugs and other over-the-counter herbal therapies and drugs, especially decongestants and sodium-based antacids

Monitoring for changes in HF signs and symptoms; what to do if symptoms worsen (first person to call for all issues or when to call which member on the team)

Rationale for activity and exercise; easy warm up/cool down exercises; getting started; when to stop or slow down

95

Barriers to Self-Care Management

96

Lack of knowledge

Literacy

Multiple medications

Fear of medication side effects

Living alone (lack of social support)

Memory problems

Higher acuity

Multiple needs

Co-morbidities

Shorter LOS

Noncompliance

Transportation issues

Financial concerns

Depression / anxiety


Education Content

The Big Picture

What HF is, its causes and symptoms, timeline (chronic), consequences (poor prognosis; premature death; greater risk for hospitalization) and measures to control it (self-care actions and monitoring)

Why drugs are used in HF; how they improve survival or reduce symptoms; common side effects and what to do when they occur; how to take medications for greatest effectiveness

98


Medications

Don’t wait until discharge!

Include the person who will assist with medication What is the plan for filling prescriptions? What is the system for medication administration

used at home?

Need to know trade/generic names Issue of medication reconciliation Use of instruction sheets versus labeled pill bottles

Don’t use term “meds as at home”

99

Medications Alternatives for routine schedule Diuretics after errands Flexible diuretic dosing ACE inhibitor at night

Discussion regarding medications to avoid

Non-steroidals

Adherence history Financial concerns Need to understand the progress made with HF management Need to understand the importance of not running out of their medication Regular follow-up with provider to monitor labs, etc.

100


Fluid Volume Status

Causes of intravascular volume overload; can occur silently (without symptoms)

Role of excess sodium in fluid retention

How diuretics work

Rationale for BID dosing if CKD

Role of additional thiazide diuretic

Need to know when NOT to take diuretics 101

Daily Weights

• Use same scale, same amount of clothing

• Empty bladder and before breakfast

• Record on calendar

• Report 2 pounds in one day or 3 to 4 pounds in a week

• Many patients don’t call because they feel “OK

• Barriers due to confusing fluid gain from fat gain

• Telephone based weight recordings or device data

• Do you weight all patients with heart failure daily while hospitalized even when admitted for non cardiac reasons?

• Special considerations with ECF

102


Response to Symptoms

Focus on changes! Is there a change in their activity tolerance?

Impact on their ADL’s?

Pants are becoming tight?

Unable to sleep lying flat?

103

Diet and Nutrition

Moderate sodium restriction Exact amount is not known

2 to 3 gram reasonable?

Most have moderate restriction when attempting to diurese

May liberalize when nutrition or orthostatic hypotension is a concern

Nutritional support for cardiac cachexia Caloric supplementation

Limit alcohol

104


Low Sodium Tips

“Low” sodium considered to be <4 grams / day

2-3 grams / day recommended for patient with clinical syndrome of heart failure < 2 grams with moderate to severe heart failure

Discuss how sodium impacts fluid retention

Salt = sodium

Focus on what they can eat

High sodium foods Approximately 70% of sodium

intake comes from processed and pre-packaged foods.

Some never or hardly every foods

105

Low Sodium Tips

Dining at restaurants or in another person’s home

Reading labels

Salt used in cooking

Sodium alternatives

Be realistic – there must be joy in life

AHA: Eat Less Salt resource book

Teach people how to do rather than tell them what to do!! 106


Fluid Limitation

In the outpatient fluid restrictions reserved for patients with advanced heart failure refractory to high dose oral diuretics

Indicated in the hospital setting in the presence of severe hyponatremia Sodium level < 130 mEq/L

Explain the thirst mechanism

107

Activity

Screen for depression

Evaluate anxiety levels

Exercise training should be considered for all stable outpatients with chronic HF who are able to participate in protocols needed to produce physical conditioning. Get them in Cardiac Rehab if possible

30 minutes moderate activity / exercise 5 days per week

Work if able 108


Follow Up

• Contact within 48-72 hours

• Appointment within on week from discharge

• Will need to have actual date, time and location included in discharge instructions

• Allows for up titration of medications

• Continues evaluation for progression of disease Need for ICD

Need for CRT

109

IS THERE ONE CORRECT ANSWER?


Nearly 2 million Medicare patients readmitted

within 30 day of discharge

Cost of those readmissions = $17.5 BILLION

National average for readmission 19%

Readmissions a symptom of an overly expensive and uncoordinated healthcare system Limited connection from inpatient to outpatient

HF readmissions rate 20-25% at 30 days > 50% at 6 months

35% of 30 day readmissions due to HF

Readmission Data

Readmissions are prevalent and costly Adverse events associated with hospital discharge are common And about ¼ of them are readmissions

Patients are not taking ideal medication regimens No f/u on meds, tests and workups is common Real room for improving hospital-receiver communication But value of PCP f/u unclear – probably varies Might not be as powerful as hospitalist f/u

Creating the perfect in-house discharge process probably won’t make enough difference

SES is probably related to readmission risk But the CMS measures do not adjust for it

Ideal risk identification strategies are unavailable.. Clinicians often have a different perspective on what led to the readmission

than patients do

What We Know


Multidimensional Nursing Roles

Coordinate care with interdisciplinary team members who can target coexisting medical, social, and financial issues

Facilitate behavioral strategies that ease patient and caregiver burdens related to adherence to the treatment plan

Educate on advance directive planning and community services that meet learning needs

Promote continuity of care between home, HF clinic, or palliative care services Foster collaborative relationships Coach collaborators to use evidence-based therapies Ensure open communication Position patients and caregivers to proactively assess and manage signs and symptoms of

worsening condition

Assess goal progression Recognize and target unresolved HF issues

113

Systematic review 47 trails

At 30 days a high intensity home-visiting program reduced all cause readmissions

At 3-6 months home-visiting programs and multidisciplinary heart failure clinic (MDS-HF) interventions reduced all cause readmissions

Structured telephone support (STS) reduced HF specific readmissions but not all cause readmissions

Mortality benefit with MDS-HF clinic, Home-visiting programs, and STS

Based on current evidence, telemonitoring interventions and primarily educational interventions are not efficacious for reducing readmissions or mortality

Transitional Care Interventions Feltner, C., Jones, C. D., Cené, C. W., Zheng, Z. J., Middleton, J. C., & Jonas, D. E. (2014). Transitional Care Interventions to Prevent Readmissions for Persons With Heart Failure. Ann Intern Med, 160, 774-784.


Final Thought They may forget your

name, but they will never

forget how you made

them feel.

-Maya Angelou

116

BE THE BEST THAT YOU CAN BE

EVERY DAY. YOUR PATIENTS ARE

COUNTING ON IT!

Documents

“I’m not telling you it is going to be easy, I’m telling you it is going …€¦ · · 2015-02-16 1 Cynthia Webner DNP, RN, CCNS, CCRN-CMC, CHFN Karen Marzlin DNP, RN, CCNS,