“i’m not telling you it is going to be easy, i’m ... · pdf filenursing...

CNEA / Key Choice

2017

Cardionursing.com 1

Karen Marzlin DNP, RN, CCNS, ACNPC-AG, CCRN-CMC, CHFN Cynthia Webner DNP, RN, CCNS, ACNPC-AG, CCRN-CMC, CHFN

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“I’m not telling you it

is going to be easy, I’m

telling you it is going

to be worth it.”

~ Art Williams

CNEA / Key Choice

2017

Cardionursing.com 2

• Offered by the American Association of Heart Failure Nurses – AAHFN

• Requirements: – Current active RN License for at least 2 years or

equivalent (4,160 hours)

– 1,200 of those hours within the past 2 years

– 30 hours of continuing education within the past 2 years

• Minimum of 15 hours must be focused on the care of patients with heart failure

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• Developed for nurses no longer in the direct care of patients with heart failure but still impact the heart failure population. – Educators, researchers, Industry reps

• RN with a BSN or equivalent bachelors degree + 2400 hours experience in current role or Masters + 2080 hours experience in current role

• Provide evidence of how nurses are indirectly involved in patients with HF or how nurses complete action(s) in their role that are related to HF

• Must have 30 hours of heart failure continuing education within the last two years.

• Same exam as the CHFN

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CNEA / Key Choice

2017

Cardionursing.com 3

• Computer based testing offered 1st, 3rd and 4th quarter of the year.

• Pen and paper test offered at the annual meeting (2nd quarter)

• 100 test questions

• Based off 2013 ACC/AHA Heart Failure Guidelines

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• Active RN license and current HF Certification

• Minimum of 600 hours in hands on heart failure clinical practice

• 40 hours of CE (past 3 years) focused on heart failure

• Complete one of the following

– Publish one CV manuscript in peer-reviewed journal as 1st author

OR

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CNEA / Key Choice

2017

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Completed 2 of the following or 1 of the following 2 times: • Published 1 clinical/professional article in a cardiovascular newsletter • Provided a formal lecture (1 hr) on a cardiovascular topic • Developed a program, service, or tool that is used in the

management of patients with heart failure • After submitting an abstract and having it accepted by a peer-review

process, presented a poster on a heart failure care topic at a local, regional, or national conference

• Earned 3 academic (college) credits in topics related to professional nursing

• Served in a leadership role with a professional society (committee, task force, board service)

• Actively participated in a quality improvement project related to heart failure care

• Co-author of a published cardiovascular manuscript (not first author) • 10 hours of continuing education in topics focused on care of

patients with heart failure within the last three years (note, this is in addition to the 40 hour minimum requirement)

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• Active RN license and current HF Certification

• Minimum of 600 hours in hands on heart failure clinical practice

• 30 hours of CE (past 3 years) with 15 hours focused on heart failure

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CNEA / Key Choice

2017

Cardionursing.com 5

I. Assessment 32 Questions A. History

B. Symptoms

C. Physical Assessment

D. Lab Tests

E. Cardiac / Pulmonary Tests

II. Planning 7 Questions A. ACC/AHA Staging and NYHA Functional Class

B. Integrate assessment into the plan of care

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I. Implementation 41 Questions A. Pharmacologic Treatment B. Non –pharmacologic Strategies C. Recommended Patient Referrals

II. Evaluation 12 Questions A. Evaluate effectiveness of therapies B. Evaluate effectiveness of teaching

III. Professional Items 8 Questions A. Demonstrate professionalism B. Maintain and improve performance

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CNEA / Key Choice

2017

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• 20% of American > 40 will develop HF in their lifetime

• > 650,000 new cases are diagnosed annually • 6.5 million people in US have HF (AHA Heart Disease and

Stroke Statistics 2017)

• Incidence increases with age – 20/1,000 people age 65-69 – > 80/1,000 people > 85 years

• Projected to increase to 8 million by 2030 • 8.5 of deaths annually in US are attributable to

HF

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2017

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• Blacks have highest risk for HF

– Associated with a greater 5 year mortality than whites

• Lowest rate of HF among white women

• Mortality rate still 50% at 5 years from diagnosis

• HF is primary diagnosis in > 1 million hospitalizations annually

• 1 month readmission rate 25%

• Total cost of HF care annually > $30 billion

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CNEA / Key Choice

2017

Cardionursing.com 8

• 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

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• 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 16

CNEA / Key Choice

2017

Cardionursing.com 9

• Dilated Cardiomyopathies (DCM)

• Familial Cardiomyopathies – 20-35% of idiopathic DCM

• Endocrine / Metabolic – Obesity – Diabetic – Thyroid – Acromegaly / Growth

Hormone Deficiency

• Toxic Cardiomyopathies – Alcoholic – Cocaine – Related to cancer treatments – Other toxins

• Sarcoidosis

• Tachycardia- Induced Cardiomyopathy

• Myocarditis and Inflammatory Processes – Myocarditis – Acquired Immunodeficiency

Syndrome – Chagas disease

• Inflamation-Induced CM: Non-infectious – Hypersensitivity Myocarditis – Rheumatological/Connective

Tissue Disorders

• Peripartum CM • CM due to Iron overload • Amyloidosis 17

DEFINITIONS

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CNEA / Key Choice

2017

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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. 19

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CNEA / Key Choice

2017


• 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 21

• 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

Primarily disease of elderly women with HTN 22

CNEA / Key Choice

2017


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

ejection fraction with no valve disease.

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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


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

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CNEA / Key Choice

2017


• At high risk for HF but without structural heart disease or symptoms of HF

• Hypertension

• CAD

• Diabetes

• Obesity

• Metabolic Syndrome

OR

• Using cardiotoxins

• Family history of Cardiomyopathy

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• Structural heart disease but without signs or symptoms of HF

• Previous myocardial infarction

• LV remodeling including left ventricular hypertrophy and low ejection fraction

• Asymptomatic valvular heart disease

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CNEA / Key Choice

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• Structural heart disease with prior or current symptoms of HF

• Known structural heart disease and HF signs and symptoms

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• Refractory HF • Marked HF symptoms at rest

• Recurrent hospitalizations despite Guideline Directed Medical Therapy

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CNEA / Key Choice

2017


I

No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF.

II

Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in symptoms of HF.

III

Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes symptoms of HF.

IV Unable to carry on any physical activity without symptoms of HF, or symptoms of HF at rest.

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I No limitation of physical activity. Ordinary physical activity does not cause fatigue, palpitations or shortness of breath.

II Slight limitation of physical activity. Comfortable at rest, but physical activity results in fatigue, palpitation or shortness of breath.

IIIa Limitation of physical activity. Comfortable at rest, but ordinary activity causes fatigue, palpitations or shortness of breath

IIIb Significant limitation of physical activity. Comfortable at rest, but minimal activity causes fatigue, palpitations or shortness of breath.

IV Unable to carry on any physical activity without discomfort or symptoms of HF at rest. 30

CNEA / Key Choice

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• 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

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CNEA / Key Choice

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The Real Culprit: Neurohormonal Response

SNS Response

RAAS Response

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Autonomic Nervous System

Sympathetic

Beta 1

HR

Contractility

Conductivity

Beta 2

Bronchodilation

Arterial Vasodilation

Alpha 1 Arterial

Vasoconstriction

Parasympathetic Vagal Response HR 34

CNEA / Key Choice

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• 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

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• 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.

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CNEA / Key Choice

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• 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

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• Enhanced preload increases end-diastolic volume dilating the LV

• LV becomes overstretched

• LV changes size and shape (ventricular remodeling)

• Contractility decreases • Congestive symptoms

develop 39

• Process of pathological growth

• Can occur from prolonged activation of SNS/RAAS

• Involves Hypertrophy of myocytes

Increased Pressure Thicken myocytes (concentric)

Increased Volume Elongate myocytes(eccentric)

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Eccentric Hypertrophy

Concentric Hypertrophy

CNEA / Key Choice

2017


Preprogrammed cell death without inflammation/scarring (necrosis)

Process is accelerated in HF but in a random pattern

Cell slippage

Bricks – myocytes

Morter – collagen Degredation (slippage) or

Fibrotic 41

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

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CNEA / Key Choice

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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

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RV Dysfunction Secondary to LV Dysfunction

• Chronic left HF is most common cause of RV failure – RV dysfunction more common in non ischemic etiology – RVEF is a predictor of mortality in patients with left HF

• LV failure leads to increased RV afterload – first from elevated pulmonary venous pressures then ultimately elevated pulmonary artery pressures

• Same pathophysiology resulting in LV failure may affect RV • Ischemia may affect both ventricles • LV dysfunction may lead to decreased systolic driving pressure

of RV coronary perfusion • Ventricular interdependence due to septal dysfunction may

occur • LV dilatation in a confined pericardial space may restrict RV

diastolic function 44

CNEA / Key Choice

2017


Pathophysiology of Right Ventricular Failure

• In response to increased pulmonary artery (PA) pressures – Initial adaptive hypertrophy; followed by progressive

contractile dysfunction

– Chamber enlargement allows for compensation for increased preload and maintenance of stroke volume (SV)

– Pulmonary hypertension may cause • RV ischemia

• Microvascular endothelial cellular dysfunction

• Apoptosis of myocytes

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Pressure Overload

Volume Overload Ischemia and

Infarction

Intrinsic Myocardial

Disease

● Left sided HF ● Mitral stenosis ●Pulmonary embolus ●Other causes of

pulmonary hypertension

● Tricuspid regurgitation ● Pulmonic regurgitation ● Mitral regurtitation ● Atrial septal defect

● RV myocardial infarction (RV is very resistant to irreversible ischemia, can regain systolic function)

● HF ● Arrhythmogenic RV

dysplasia ● Sepsis

Inflow Limitation

Congenital Pericardial

Disease

● Tricuspid stenosis ● Ebstein's anomaly ● Tetralogy of Fallot ● Transposition of great

arteries

● Constrictive pericarditis

Causes of Right Heart Failure (Examples)

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CNEA / Key Choice

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Response to Failing RV

• Neurohormonal, endothelin and cytokine activation

– SNS adversely affects RV remodeling

– RAAS activation affects RV remodeling and contributes to fluid retention

– Endothelin I levels in pulmonary arterial hypertension are associated with more severe RV dysfunction and decreased exercise capacity

– Increased levels of tumor necrosis factor and endotoxin are associated with more symptomatic disease

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Decompensated RV Failure

• Rising filling pressures

• Diastolic dysfunction of LV – RV dilation or pressure overload causes leftward shift of

septum and impacts LV function

• Decreased cardiac output – PA pressures may actually decrease in severe RV failure

due to decreased CO of RV

• Tricuspid valve regurgitation – Annular dilatation and poor leaflet coaptation – Aggravates volume overload and further decreases RV

forward flow

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CNEA / Key Choice

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Manifestations of RV Failure

• Fluid retention – JVD – + Hepatojugular Reflex – Peripheral edema – Ascites

• Cardiac cirrhosis in severe cases

– Anasarca

• Decreased systolic reserve (decreased C.O.) – Decreased exercise tolerance

• Exercise capacity may be one of most important prognostic factors

– Fatigue

• Cardiac arrhythmias

– Atrial most common

• Protein losing enteropathy

– Severe loss of proteins into the intestine

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RV Dysfunction and Prognosis

• RV function is the most important determinant of longevity in patients with pulmonary arterial hypertension (PAH)

• In left ventricular failure, RV failure may be final common pathway and thus sensitive indicator for impending decompensation and poor prognosis

• Severity of tricuspid regurgitation correlates with worse survival

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CNEA / Key Choice

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Exercise intolerance (hallmark) – Assess NYHA Inability to perform ADLs, Fatigue, Dyspnea

Paroxysmal nocturnal dyspnea attacks of severe shortness of breath and coughing that

generally occur at night. It usually awakens the person from sleep, and may be quite frightening

Orthopnea shortness of breath (dyspnea) which occurs when lying flat

Bendopnea Shortness of breath when bending forward for 30 seconds

Frequent night urination with less during the day Peripheral edema/weight change/increase

abdominal girth Chest pain GI problems Confusion/altered mental status

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CNEA / Key Choice

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• Symptoms in the elderly

Many don’t experience exertional dyspnea because they are sedentary

More common:

Daytime oliguria/nocturia

Mental disturbances

Anorexia

GI disturbances

Clinical Pearl: Ask about the last time the patient felt really well. What activities were they doing then?

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• General Appearance (resting dyspnea, cyanosis, cardiac cachexia)

• Weight gain • JVD • Hepatojugular reflux • Edema • Displaced apical impulse • S3/S4 • BP/HR

– Include orthostatic pressures

• Murmurs – MR, AS, AR • Lung sounds

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CNEA / Key Choice

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Preload • The ventricle is preloaded with

blood at the end of diastole: Creates stretch on myocardial muscles fibers

• Determined by: – Volume of blood filling the ventricle at

end of diastole – Greater the volume the greater the

stretch (muscle fiber length) – Greater the stretch the greater the

contraction – Greater the contraction the greater

cardiac output

TO A POINT

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• JVD • Hepatojugular reflux

• Less specific

– Peripheral edema – Weight

•Dyspnea / increased work of breathings •Hypoxemia (Diffusion abnormality) •Orthopnea / bendopnea (flexopnea) •CXR •BNP / NT-proBNP •Lungs sounds – Role of lymph drainage – Clear lungs do not rule out volume

overload •S3 or S4

•Less specific – Blood Pressure – Urine Output – Weight 56

CNEA / Key Choice

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Invasive Assessment • RA Pressure

– CVP or Central Venous Pressure

• Direct measurement of pressure in right atrium

• Normal < 6mm Hg

Invasive Assessment

• PCWP – Pulmonary Capillary Wedge Pressure

• Indirect measurement of left atrial pressure

• – Normal < 15 mm HG

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Measuring level of JV Pulsation (JVP)

• Raise HOB 30 – 45 degrees – 45 degree angle will

cause venous pulsation to rise 1 to 3 cm above the sternal angle

• Internal jugular preferred

• May use external

• Use tangential light

• Use centimeter ruler

• Difficult to assess if HR>100

• Normal JVP level is < 3 cm above the sternal angle

• Sternal angle is 5cm above

right atrium • JVP of 3 cm + 5cm =

estimated CVP or right atrial pressure of 8cm H2O

• Estimated CVP / right atrial

pressure > 8 cmH2O – Usually RV failure – Tricuspid valve regurgitation – Pulmonary hypertension

CNEA / Key Choice

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JVD (Jugular Venous Distension)

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No pulsations palpable. Palpable pulsations.

Pulsations obliterated by pressure above the clavicle.

Pulsations not obliterated by pressure above the clavicle.

Level of pulse wave decreased on inspiration; increased on expiration.

No effects of respiration on pulse.

Usually two pulsations per systole (x and y descents).

One pulsation per systole.

Prominent descents. Descents not prominent.

Pulsations sometimes more prominent with abdominal pressure.

No effect of abdominal pressure on pulsations.

• Additional assessment for increased volume or pressure.

• An evaluation of neck vein distention occurs while assessing HJR so patient position is the same as with JVD assessment.

• Apply firm pressure over the liver (right upper quadrant of the abdomen) for approximately 30 seconds.

• A more pronounced rise in JVD indicates a positive test.

• Positive HJR indicates: – Increased preload/hypervolemia – Right ventricular failure

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CNEA / Key Choice

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• Note location of edema

• Edema may be in dependent locations, such as the sacrum in the recumbent patient.

• Evaluate men for scrotal edema.

• Described as pitting or non-pitting

• Anasarca: generalized edema

• Evaluated on a 5-point scale – 0 = No edema present

– 1+ = 0 to ¼ inch, Trace

– 2+ = ¼ to ½ inch, Mild

– 3+ = ½ to 1 inch, Moderate

– 4+ = > than 1 inch, Severe

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Source: http://www.med-health.net/Edema-Grading.html

CNEA / Key Choice

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Cardiac Ascites

• Congestive hepatopathy and chronic passive liver congestion are more accurate terms than cardiac cirrhosis – Abnormal PT is common – Most common liver enzyme abnormality is elevated

bilirubin • Abnormalities seen with right atrial pressures > 10 mmHg

– Need to differentiate from ischemic hepatitis • Caused by cardiogenic shock • Associated with more extreme elevations in AST and ALT

• Paracentesis – High serum – ascites albumin gradient (SAAG) greater than

1.1 g/dL – High ascitic fluid total protein > 2.5 g/dL – Hepatic albumin synthetic function is usually preserved so

parental albumin is not necessary

Hepatic Ascites

• Portal HTN in presence of liver cirrhosis – Chronic alcohol use or viral hepatitis

• Hypoalbuminemia usually present • Paracentesis

– High serum – ascites albumin gradient (SAAG) – Only 10% of time have a high ascitic fluid total protein > 2.5

g/dL. – Need for parental albumin supplementation after paracentesis

• Other causes of ascites: Infective, inflammatory and infiltrative conditions

CNEA / Key Choice

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Edema Differentials

Nephrotic Syndrome

• Nephrotic-range proteinuria • single spot urine: 2 g of protein

per gram of urine creatinine

• Hypoalbuminemia

• Edema

Lymph Edema

• Abnormal collection of protein-rich fluid in the interstitium resulting from obstruction of lymphatic drainage

• Diagnosis based on exclusion of other causes of edema – Heart failure, renal failure,

hepatic failure, and venous stasis.

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CNEA / Key Choice

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• Orthostatic hypotension is a systolic fall of at least 20 mm Hg or a diastolic fall of at least 10 mm Hg within three minutes of standing.

• Procedure for assessing orthostatic blood pressure: – All requirements for normal blood pressure assessment should

be followed including cuff size, arm position etc. – Measure lying blood pressure after the patient has been supine

for a minimum of 5 minutes. – Stand the patient. Measure the blood pressure after the patient

has been standing for one minute. – If the patient can continue to stand, measure the blood pressure

at 3 minutes and again at five minutes. – Note any symptoms the patient experiences. – If the patient is unable to stand for 3 minutes measure the

blood pressure at 1 and 2 minutes if able. – Record the blood pressure, any symptoms and the time intervals

of the standing pressures. 69

• Closure of the Mitral (M1) valve and the Tricuspid (T1) valve

• Beginning of Ventricular Systole and Atrial Diastole

• Location: Mitral area

• Intensity: Directly related to force of contraction

• Duration: Short

• Quality: Dull

• Pitch: High

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CNEA / Key Choice

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• Closure of Aortic (A2) and Pulmonic (P2) Valve

• End of Ventricular Systole

• Location: Pulmonic area

• Intensity: Directly related to closing pressure in the aorta and pulmonary artery

• Duration: Shorter than S1

• Quality: Booming

• Pitch: High 71

• Early diastolic filling sound

• Caused by increased pressure and resistance to filling.

• Most frequently associated with systolic dysfunction

• Associated with: – Fluid overload state

– Right or left ventricular failure

– Ischemia

– Aortic regurgitation

– Mitral regurgitation

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CNEA / Key Choice

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• Patient position: left lateral decubitus position

• Location: – Left-sided S3 – mitral area. – Right-sided S3 – tricuspid area.

• Intensity – Left-sided heard best during

expiration. – Right-sided heard best during

inspiration.

• Duration: short. • Quality: dull, thud like. • Pitch: low. • May be normal in children, young

adults (up to 35-40) and in the 3rd trimester of pregnancy.

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• Late diastolic filling sound • Caused by atrial contraction and the

propulsion of blood into a noncompliant (stiff) ventricle.

• Most frequently associated with diastolic dysfunction

• Associated with:

– Fluid overload state – Systemic hypertension – Restrictive cardiomyopathy – Ischemia – Aortic stenosis – Hypertrophic cardiomyopathy

• May be normal in athletes 74

CNEA / Key Choice

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• Patient position: left lateral decubitus position.

• Location

– Left-sided S4 – mitral area. – Right-sided S4 – tricuspid

area. • Intensity

– Left-sided louder on expiration.

– Right-sided louder on inspiration.

• Duration: Short • Quality: Thud like • Pitch: Low

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Afterload

• After the ventricle is loaded: • Pressure ventricle needs to

overcome to eject blood volume

• Systemic vascular resistance is major component of left ventricular afterload – Other components

• Valve compliance • Arterial wall compliance • Viscosity of blood

•Pulmonary vascular resistance is major component of right ventricular afterload

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CNEA / Key Choice

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Afterload Assessment

• Left ventricle: –Pulse pressure and

DBP • Normal pulse pressure

35 to 40

• Right ventricle: –Hypoxemia –Positive pressure

ventilation / PEEP

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Contractility

• Ability of myocardium to contract independent of preload or afterload

–Inotropic state

• Related to degree of myocardial fiber stretch (preload) and wall tension (afterload).

• No accurate way to measure contractility

• Contractility influences myocardial oxygen consumption

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Noninvasive Assessment: Ejection Fraction

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• CBC • UA • Electrolytes – including magnesium and calcium • BUN / Creatinine • Glucose • Fasting lipid profile • Liver function studies • Albumin • Thyroid stimulating hormone

– Diagnose new disease or evaluate the effectiveness of current treatment

• Cardiac Biomarkers: Troponin

BNP / NT proBNP Diagnosis and Prognosis

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• Lower levels than NT-pro-BNP

• Cleared more quickly from the circulation – 20 minutes

• Cleared by natriuretic peptide receptors

• Higher levels than BNP

• Cleared more slowly from the circulation- 120 minutes

• Cleared by various organs – Skeletal tissue, liver, kidneys

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Both equally cleared by kidneys Both equally useful in the diagnosis of acute decompensated heart failure Both may be elevated for reasons other than HF

• Good to assess in patients with dyspnea being evaluated for Heart Failure

• Should not be used as the sole tool to diagnose HF

• Must be used in concert with signs and symptoms

• Low values have strong negative predictive value

• Adds to prognostic information – marker of risk

• Predictor of increased risk

– If levels do not fall after aggressive HF care, risk for death or hospitalization for HF is significant (ACC/AHA 2013)

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CNEA / Key Choice

2017


• < 100 pg/mL - HF unlikely

• > 400 pg/mL - HF likely

• 100-400 pg/mL - Use clinical judgment

• < 300 ng/mL - HF unlikely

• Age < 50 years, NT-proBNP >450 pg/mL - HF likely

• Age 50-75 years, NT-proBNP >900 pg/mL – HF likely

• Age >75 years, NT-proBNP >1800 – HF likely

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Cardiac • Heart failure, including RV

syndromes

• Acute coronary syndrome

• Heart muscle disease, including LV Hypertrophy

• Valvular heart disease

• Pericardial disease

• Atrial fibrillation

• Myocarditis

• Cardiac surgery

Non-cardiac • 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

environmental 85

CNEA / Key Choice

2017


• Hyponatremia occurs with volume overload

• Hyponatremia occurs with thiazide diuretics / aldosterone antagonists

• Diuretics predispose to hypokalemia

• Aldosterone antagonist are potassium sparing and can increase risk for hyperkalemia – Spironolactone

– Epleranone

• Certain salt substitutes contain potassium

86

• Hypochloremic metabolic alkalosis – Low serum chloride

– High serum CO2

– May result from hypovolemia

• Serum value correlates with the bicarb on an arterial blood gas

• Low serum CO2 can be indicative of metabolic acidosis

• High serum CO2 can be indicative of metabolic alkalosis

• Venus pH can confirm acidosis

87

CNEA / Key Choice

2017


• Elevated BUN

• Kidney failure

• Dehydration

• GI bleeding

• Protein catabolism

• Acute kidney injury

– Increase in creatinine of > 0.3 mg/dL within 48 hours

– Increase in creatinine > 1.5 x baseline within last 7 days (known or presumed)

• Creatinine of 2.0 (females) and 2.5

(males) cut off for use of aldosterone antagonists

• Creatinine of 3.0 is general cut off for use of ACE inhibitors / angiotensin receptor blockers in chronic kidney disease (CKD)

88

Diuretics and Renal Function

• Role of venous congestion in worsening renal function

• Role of volume depletion / hypotension and worsening renal function

89

CNEA / Key Choice

2017


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)

90

MULLENS, W., ABRAHAMS, Z., FRANCIS, G. S., SOKOS, G., TAYLOR, D. O., STARLING, R. C., ... & TANG, W. W. (2009).

IMPORTANCE OF VENOUS CONGESTION FOR WORSENING OF RENAL FUNCTION IN ADVANCED DECOMPENSATED HEART FAILURE. JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 53(7), 589-596.

We observed in our patient population with low-output decompensated HF that besides the presence of intrinsic renal insufficiency, venous congestion was the strongest hemodynamic determinant for the development of WRF. In contrast, impaired CI on admission and improvement in CI after intensive medical therapy had a limited contribution to WRF.

91

CNEA / Key Choice

2017


Increased CVP is associated with impaired renal function and independently related to all-cause mortality in a broad spectrum of patients with cardiovascular disease.

92

DAMMAN, K., VAN DEURSEN, V. M., NAVIS, G., VOORS, A. A., VAN VELDHUISEN, D. J., & HILLEGE, H. L. (2009). INCREASED CENTRAL VENOUS PRESSURE IS ASSOCIATED WITH IMPAIRED RENAL FUNCTION AND MORTALITY IN A BROAD SPECTRUM OF PATIENTS WITH CARDIOVASCULAR DISEASE. JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 53(7), 582-588.

• Assess for hyper or hypothyroidism

• Anemia results in decrease oxygen carrying capacity

• Goes hand in hand with renal dysfunction

• Iron studies, ferritin to evaluate for iron deficiency

93

CNEA / Key Choice

2017


• May elevate secondary to passive liver congestion

• Passive liver congestion can also lead to alteration in PT/INR

94

• Ischemia

• Arrhythmias

• Hypertrophy

• Drug side effects

• Conduction abnormalities – Bundle branch block

– QT interval

95

CNEA / Key Choice

2017


• Chest x-ray

– Assess heart size

– Pulmonary congestion

– Detect alternative cardiac , pulmonary and other diseases that may cause or contribute to the symptoms

96

97

• Prominent vascular markings: upper lung fields

• Kerley B lines

• Peribronchial thickening

• Patchy alveolar filling in a perihilar distribution – progressing to diffuse infiltrates

CNEA / Key Choice

2017


98

• LV Function /RV Function

• LV size /RV size

• Wall thickness

• Wall motion

• Valve function

• Atrial size

• Pulmonary artery systolic pressure

• Serial studies important to assess response to therapy

• Routine studies without changes in therapy or condition not recommended

• MRI – LV volume and LVEF

– Myocardial perfusion and viability

– Myocardial fibrosis

– Identify congenital disease

• CT Scan – Cardiac structure & function

– Including coronaries

• Stress test – For those with known CAD

and no angina to assess for ischemia

99

CNEA / Key Choice

2017


• Cardiac Catheterization – Patients with high suspicion for obstructive CAD – Rule out CAD as a cause for newly diagnosed LV dysfunction

• Invasive Hemodynamic Assessment (Right Heart Cath) – To guide therapy in patients in whom the adequacy or excess of

intracardiac filling pressures cannot be determined from clinical assessment.

– Assessment of cardiac output – Right heart pressures – To differentiate pulmonary hypertension from LV failure vs

Pulmonary arterial hypertension • PA pressures • PCWP

100

TREATMENT STRATEGIES

101

CNEA / Key Choice

2017


Stages, Phenotypes and Treatment of HF






symptoms of HF

THERAPY

Goals

· Control symptoms

· Improve HRQOL



Strategies


Treatment


of congestion








symptoms of HF







THERAPY

Goals



remodeling

Drugs

· ACEI or ARB as

appropriate

· Beta blockers as

appropriate


· ICD


valvular surgery as

appropriate




HFpEF HFrEF

THERAPY

Goals



coronary disease


abnormalities

Drugs

· ACEI or ARB in






of-life goals










rest


despite GDMT


· Previous MI


LVH and low EF


disease


· HTN


· DM

· Obesity


or

Patients



cardiomyopathy

Development of


disease

102

• Heart healthy lifestyle

• Prevent vascular, coronary disease

• Prevent LV structural abnormalities

• HTN screening / treatment

• ACE I or ARB in appropriate patients with vascular disease or DM

• Statins per recommendations for primary prevention

• Risk factor modification – Diet

– Exercise

– Tobacco cessation

103

CNEA / Key Choice

2017


• Structural heart disease but without signs or symptoms of HF

• Medications to prevent ventricular remodeling – Beta blockers

– ACE inhibitors / ARBs

– Aldosterone antagonist

• ICD

• Revascularization

• Valvular surgery

104

• Control symptoms

• Patient education

• Prevent hospitalization

• Prevent mortality

• Diuretics for fluid retention

• Beta blockers

• ACE I or ARB

• Entresto (Neprilysin inhibitor (sacubitril) with ARB (valsartan)

• Aldosterone blockers

• Hydralazine/isosorbide dinitrate

• Digoxin

• Corlanor

• CRT

• ICD

• Revascularization or valvular surgery as appropriate

• Palliative care partnering with guideline directed medical therapy

105

CNEA / Key Choice

2017


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. 106


• Improve quality of life



• Diuresis to relieve symptoms of congestion

• Identify comorbidities

• Follow guideline driven indication for comorbidities

– HTN, AF, CAD, DM, sleep apnea, anemia

• Revascularization or valvular surgery as appropriate

107

CNEA / Key Choice

2017



• Improve quality of life



• Advance care measures

• Heart Transplant

• Chronic inotropes

• Temporary or permanent mechanical circulatory support

• Experimental surgery or drugs

• Palliative care and hospice

• ICD deactivation

108






symptoms of HF

THERAPY

Goals

· Control symptoms

· Improve HRQOL



Strategies


Treatment


of congestion








symptoms of HF







THERAPY

Goals



remodeling

Drugs

· ACEI or ARB as

appropriate

· Beta blockers as

appropriate


· ICD


valvular surgery as

appropriate




HFpEF HFrEF

THERAPY

Goals



coronary disease


abnormalities

Drugs

· ACEI or ARB in






of-life goals










rest


despite GDMT


· Previous MI


LVH and low EF


disease


· HTN


· DM

· Obesity


or

Patients



cardiomyopathy

Development of


disease

109

CNEA / Key Choice

2017


• No evidence based medical therapy • ARBs, aldosterone antagonists, and sildenafil have all

been tested • ARBs and aldosterone antagonists may reduce

hospitalizations but not mortality • TOPCAT Study • Focus on co-morbid conditions:

– Hypertension – Diabetes – Sleep apnea – Atrial Fibrillation - arrhythmias – Renal dysfunction

110

• Treatment of Preserved Cardiac Function HF with Aldosterone Antagonist – published 2014

• Randomized 3,445 patients to spironolactone or placebo – 1678 from Russia/Georgia – 1767 from US,Canada, Brazil, Argentina (Americas)

• Primary composite outcome: Time to CV death, aborted cardiac arrest, or hospitalization for management of HF

• No statistically significant benefit to spironolactone Pitt B, et al. TOPCAT Investigators. Spironolactone for heart failure with preserved

ejection fraction. N Engl J Med. 2014;370:1383–1392 111

CNEA / Key Choice

2017


• 4 fold difference identified in the composite event rate between groups enrolled in Russia/Georgia compared with those enrolled in the Americas

• All clinical event rates were markedly lower in Russia/Georgia, and there was no detectable impact of spironolactone on any outcomes.

• In contrast, in the Americas, the rates of the primary outcome, cardiovascular death, and hospitalization for heart failure were significantly reduced by spironolactone.

Pfeffer, M. A.,et al. (2015). Regional variation in patients and outcomes in the Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antagonist (TOPCAT) trial. Circulation, 131(1), 34-42.

112

ACC/AHA/HFSA Guideline Update Recommendations Adldosterone Antagonist in HFpEF

COR LOE Recommendations

IIb B-R In appropriately selected patients with HFpEF (with EF ≥45%, elevated BNP levels or HF admission within 1 year, estimated glomerular filtration rate >30 mL/min, creatinine <2.5 mg/dL, potassium <5.0 mEq/L), aldosterone receptor antagonists might be considered to decrease hospitalizations (83, 166, 167).

113

COR= Class of Recommendation (strength); yellow, is reasonable/useful (Moderate) LOE = Level of Evidence (Quality); B = moderated quality; 1 or more randomized trials; GDEM: Guideline-directed evaluation and management

Yancy C, Jessup M, et al. Circulation. 2017).

CNEA / Key Choice

2017







symptoms of HF

THERAPY

Goals

· Control symptoms

· Improve HRQOL



Strategies


Treatment


of congestion








symptoms of HF







THERAPY

Goals



remodeling

Drugs

· ACEI or ARB as

appropriate

· Beta blockers as

appropriate


· ICD


valvular surgery as

appropriate




HFpEF HFrEF

THERAPY

Goals



coronary disease


abnormalities

Drugs

· ACEI or ARB in






of-life goals










rest


despite GDMT


· Previous MI


LVH and low EF


disease


· HTN


· DM

· Obesity


or

Patients



cardiomyopathy

Development of


disease

114

• Point 1: Why do we use them when they decrease contractility? – Inhibits adverse effects of SNS activation

• Decrease myocardial oxygen consumption – Decreases HR – Decreases contractility (however, benefit outweighs)

– Inhibits ventricular remodeling and apoptosis – Slows disease progression – Can improve LVEF – Decreases mortality/hospitalization – Reduce symptoms, improve clinical status, and

enhance the patient’s overall sense of well-being

115

CNEA / Key Choice

2017


• Cannot assume class effect • Bisoprolol – β1

– CIBIS III randomized trial – 2005 (enalapril)

• Metoprolol succinate - β1

– MERIT-HF randomized trial – 1999 (placebo)

• Carvedilol - β1, β2, α1

– CAPRICORN randomized trial – 2001 (placebo)

– COMET randomized trial – 2003 (metoprolol tartrate)

116

• Even better in combination with ACE Inhibitor

– Started after initiation of ACE-I but before getting to target dose of ACE-I

• Must be used with diuretic if any recent or current fluid retention

• Start very low doses with gradual up-titration

• Titration to target dose essential

When to initiate? • Do not initiate in an acutely

decompensated patient – Remember you are giving a

negative inotrope

• Can be initiated in hospital for HF admission if inotropic therapy not required

• If decompensation occurs on a beta blocker it is generally not stopped unless inotrope is needed. Dose may need to be decreased.

117

CNEA / Key Choice

2017


• Bradycardia / heart blocks

– Generally asymptomatic

– Decrease or stop: If accompanied with dizziness, light headedness, 2nd or 3rd degree heart block

• Hypotension

– Consider administration opposite of ACE-I or decrease in diuretic dose

• Erectile Dysfunction

– May be less prevalent with carvedilol

118

• Stage A

• Stage B

– All patients with a recent or remote history of MI or ACS and reduced EF to reduce mortality

• Stage C

– For all patients with current or prior symptoms of HFrEF, unless contraindicated, to reduce morbidity and mortality.

119

CNEA / Key Choice

2017


Renin-Angiotensin Aldosterone System (RAAS)

↓ Renal Blood Flow / Perfusion

Renin Release

Angiotensinogen Angiotensin I

Angiotensin Converting Enzyme

Angiotensin II

Vasoconstriction Aldosterone Release

Na+ and H2O Retention

↑ BP → ↑ Renal Perfusion

Beta Blockers

ACE Inhibitors Angiotensin

Receptor Blockers

Aldosterone Antagonists

120

A Closer Look at ACE Inhibitors and

Angiotensin II Receptor Blockers

• Angiotensin-converting enzyme inhibitors (“pril” medications)

– Captopril, Enalapril, Lisinopril, Quinapril, Ramipril, Benazepril, Fosinopril

• Angiotensin II Receptor Blockers (“sartan”

medications)

– Losartan, Irbesartan, Candesartan,Telmisartan,Valsartan, Eprosartan

121

CNEA / Key Choice

2017


A Closer Look at ACE-Is / ARBs

• Overall cardioprotective, vasculoprotective effect, and renal protective – Prevents ventricular remodeling

– Reduce mortality in patients with systolic heart failure

– Reduction of left ventricular mass in LV hypertrophy

– Slows progression of both renal disease in diabetes and hypertensive nephrosclerosis

122

• Increases bradykinin release and can produce cough – Release of bradykinin causes constriction of non-vascular

smooth muscle in bronchus – Cough is side effect in 10-20% of patients

• Need to assure cough is not sign of worsening heart failure • Patient should be changed to an angiotensin receptor

blocker (ARB) if unable to tolerate cough

123

CNEA / Key Choice

2017


• Secondary to excessive accumulation of bradykinin

• Occurs in 0.7% of treated patients • Likely genetic – non histamine angioedema • Usually soon after administration but could

occur after years of use • African Americans have a 4-5x greater risk • Women have a 2x higher risk than men • Class effect reaction:

– Absolute contraindication to further ACE I use

Treatment: Stop ACE I Antihistamines / corticosteroids not effective Epinephrine only if there is airway compromise FFP 2-4 units – suppresses bradykinin inhibits

edema progression Ecallantide- suppresses bradykinin generation Icatibant - bradykinin B2 receptor antagonist

124

Angiotensin Receptor Blockers End in “SARTAN”

• ACE Inhibitors remain the first choice for inhibition of RAAS

• ARB’s are a reasonable alternative to ACE Inhibitor if intolerant to ACE Inhibitor due to cough or angioedema

• Directly blocks angiotensin II

• ARB is a component of Entresto

• Combination of ACE I and ARB – not recommended

125 2017

CNEA / Key Choice

2017


• No absolute contraindication to ARB in patient with angioedema from ACE I • ACC/AHA/HFSA Guideline Update - ARB to be used in place of ACE I when there

has been cough or angioedema with ACE I (Yancy et al. Circulation. 2016;134)

• Risk of angioedema with ARB is low – Rate of angioedema in ARB population the same as placebo group1

– Rate of angioedema highest in ACE I group when comparing patients on ARB, betablocker and ACE I

• Equal rate of angioedema between beta blocker and ARB groups2

• In patients with history of angioedema with ACE I – 4-10% of patients who developed angioedema with ACE I have developed

angioedema with ARB3,4

– Sample sizes are small

126

1. Makani H et al. Am J Cardiol 2012 2. Toh S et al. Arch Intern Med 2012 3. Haymore et al. Ann Allergy Asthma Immunol 2009 4. Beavers, C. J. et al . Annals of Pharmacotherapy, 2012

ACE Inhibitors / ARBs and Renal Function: Sorting Out the Confusion

• Renal protective in chronic kidney disease • However, can cause acute kidney injury (AKI) in patient’s at risk

(i.e. low stroke volume) due to preventing the compensatory mechanism of efferent vasoconstriction – When there is decreased blood flow into the glomerulus via the afferent arterioles,

the efferent arterioles constrict to raise glomerular filtration pressure on the back end

– ACE-I prevent efferent vasoconstriction

• Creatinine can be allowed to be 35% above baseline without stopping the drug. – As forward flow to the glomerulus improves – there is less

need for efferent vasoconstriction to compensate and glomerular filtration will stabilize

• Will cause acute renal failure in patients with bilateral renal artery stenosis – Dilation of efferent glomerular arterioles with no ability to dilate afferent arterioles

which results in decreased glomerular filtration – In bilateral renal artery stenosis there is fixed flow into the glomerulus – an

improvement in stroke volume will not improve flow into the glomerulus •

127

CNEA / Key Choice

2017


Bowman’s Capsule (Glomerulus)

128

• Assess renal function and potassium within 1 to 2 weeks of initiation if outpatient

• High risk features for AKI

– Hypotension

– Azotemia

– Diabetes

– Hyponatremia

• High risk features for hyperkalemia

– Potassium supplementation in combination with aldosterone antagonist

Contraindications (HF Guidelines) Bilateral renal artery stenosis Creatinine > 3 mg /dL in CKD AKI (until resolved) Potassium > 5.0 mEq/L Systolic BP < 80 mmHg

May consider holding short term in patients at high risk for AKI.

129

ESRD: ACE Inhibition ok . SBP most often limiting factor. Need reasonable SBP for

dialysis.

CNEA / Key Choice

2017


• Stage A – May be beneficial in treatment of hypertension

– Renal and vascular protective in DM

• Stage B – All patients with a recent or remote history of MI or ACS

and reduced EF – prevent HF

– All patients with HFrEF

– ARBs are appropriate if intolerant of ACE I

• Stage C – All patients with HFrEF and current or prior symptoms,

unless contraindicated, to reduce morbidity and mortality

130

• New class of medication: ARNI – Angiotensin Receptor Blocker with Neprilysin Inhibitor

• Combo drug: sacubitril (Neprilysin Inhibitor) with valsartan (ARB)

• PARADIGM-HF Trial • Multinational, randomized, double-blind trial • Comparing ENTRESTO with enalapril • 8,442 adult patients with symptomatic chronic heart failure (NYHA class

II–IV) and systolic dysfunction (left ventricular ejection fraction ≤40%). • Results:

• 20% reduction in the rate of death or hospitalization for heart failure

• 16% reduction in the rate of all-cause death compared to enalapril at 3.5 years of follow-up.

131

CNEA / Key Choice

2017


Endogenous Vasoactive Peptides

• Naturetic peptides • Adrenomedullin • Bradykinin • Substance P • Calcitonin gene-related

peptide

↓ Neurohormonal activation ↓ Vascular tone ↓ Cardiac fibrosis, hypertrophy ↓ Sodium retention

N

E

P

R

I

L

Y

S

I

N

Neprilysin Inhibitor

132

133

CNEA / Key Choice

2017


134

Sacubitril / Valsartan (Paradigm HF listed doses) 24 mg/26 mg (50 mg)

49 mg/51 mg (100 mg) 97 mg/103mg (200 mg)

Valsartan in Entresto is more bioavailable in Entresto than valsartan alone.

Dosing equivalents: Valsartan In Entresto = Valsartan alone

26mg in Entresto = 40 mg alone 51 mg in Entresto = 80 mg alone

103 mg in Entresto = 160mg alone

135

CNEA / Key Choice

2017


• Do not administer with ACE I – Increased risk of angioedema

– Stop ACE I for 36 hours before starting Entresto

– Do not administer in patients with history of angioedema

• Monitor kidney function, blood pressure and potassium levels

• BNP levels will not be accurate with Entresto but pro-BNP levels may be used

136

• Hypotension 18%

• Hyperkalemia 12%

• Cough 9%

• Dizziness 6%

• Renal failure/AKI 5%

• Hypotension 12%

• Hyperkalemia 14%

• Cough 13%

• Dizziness 5%

• Renal failure/AKI 5%

137

CNEA / Key Choice

2017



I ACE I: A Inhibition of the RAS with ACE I OR ARB OR ARNI in conjunction with evidence-based betablocker, and aldosterone antagonist in selected patients, is recommended for patients with chronic HFrEF to ↓ mortality and morbidity.

ARB: A

ARNI: B-R

138

COR= Class of Recommendation (strength); green is recommended (Strong) LOE = Level of Evidence (Quality); A = high quality evidence; B = moderated quality evidence; R = randomized

Yancy C, Jessup M, et al. Circulation. 2016;134: e Pub (May 20).


I ACE I: A Use of ACE I is beneficial for patients with prior or current symptoms of chronic HFrEF to ↓ morbidity and mortality

ARB: A The use of ARB to ↓ morbidity and mortality is recommended in patients with prior or current symptoms of chronic HFrEF who are intolerant to ACE inhibitors because of cough or angioedema

ARNI: B-R In patients with chronic symptomatic HFrEF NYHA class II or III who tolerate an ACE I or ARB, replacement by ARNI is recommended to further ↓ morbidity and mortality

139

COR= Class of Recommendation (strength); green is recommended (Strong) LOE = Level of Evidence (Quality); A = high quality evidence; B = moderated quality evidence; R = randomized


CNEA / Key Choice

2017


• Mineralocorticoid Receptor Antagonist (MRA)

• Heart Failure – ACC/AHA Class IA Recommendation LVEF < 35% with NYHA Class II-IV

Heart Failure already on ACE I and BB

• STEMI – ACC/AHA Class IB Recommendation

– LVEF < 40% already receiving an ACE inhibitor and beta blocker

– Greatest impact if initiated within 7 days

Used in STEMI and HF for reduction in mortality 140

141

RALES Trial (1999) – 1663 pts • NYHA Class III-IV • LVEF < 35% • Standard rx. vs standard rx. with

spironolactone • 30% ↓ in mortality • 35% ↓ in hospitalization

EMPHASIS-HF (2011) – 2737 pts • NYHA Class II • LVEF < 35% • Standard rx. vs standard rx. with epleranone

• 24% ↓ in all cause mortality • 42% ↓ in HF hospitalization

2017

CNEA / Key Choice

2017


• Promotes retention of sodium

• Promotes loss of potassium and magnesium

• Potentiates catecholamines

• Inhibits the parasympathetic nervous system

• Decreases arterial compliance

• Promotes direct remodeling

• Has prothrombotic properties

• Causes vascular inflammation and injury

142

• Non selective aldosterone blocker – Blocks aldosterone and

androgen; stimulates progesterone

• RALES Trial

• Selective aldosterone receptor antagonist

• EMPHASIS-HF

• EPHESUS (Post MI)

Major side effect:

gynecomastia (10%), sexual

dysfunction and menstrual

problems due to non

selectivity

Eliminates most

gynecomastia and sexual side

effects associated with

aldactone

143

CNEA / Key Choice

2017


• Potassium sparing medications

• Any potassium supplements should be stopped after initiating - consider potassium based

salt substitutes

• Counsel patients about avoiding foods high in potassium

Lab Monitoring • Potassium and renal

function checked 2-3 days after initiation and again at 7 days then at the one month mark. If stable then every 3 months.

• Adding or increasing ACE I or ARB should increase potassium and creatinine surveillance.

• Also monitor for hyponatremia.

144

• Combination of fixed dose of Hydralazine & Isosorbide Dinitrate (ISDN) to a standard medical regimen for HF, including ACEIs and beta blockers, is recommended patients self-described as African Americans, with NYHA functional class III to IV HF.

• Rationale: Less renin responsive

• Morality benefit • Compliance is difficult • Target dose: 3 times a day, for a total DAILY dose of 120 mg

ISDN (40mg TID) and 225 mg hydralazine (75mg TID) • Bidil: ISDN 20mg / hydralazine 37.5mg

– 1 up to 2 tablets TID

145

Combination may also be considered in those who are ACE I or ARB intolerant.

CNEA / Key Choice

2017


• African American Heart Failure Trail (2004) - A-HeFT

• 1050 self-described African American patients

• NYHA Class III or IV

• LVEF < 35% or < 45 with a dilated left ventricle

• Currently on standard therapy with BB for at least 3 months prior to enrollment

• Randomized to standard therapy + placebo (1 tablet TID) or standard therapy + 37.5mg of hydralazine and 20mg of ISDN (combined in one tablet TID)

• Dose increased to 2 tablets TID if no side effects with 1 tablet TID

• Trial ended early due to significantly higher rate of mortality in placebo group

– 43% reduction in rate of death from any cause

– 33% reduction in the rate of first hospitalization for heart failure in treatment group

– Significant improvement in quality of life score in treatment group

146

• Initiation: • Hydralazine 37.5 mg / ISDN

20mg 3 times daily

• Target dose: – Total DAILY dose of

Hydralazine 225 mg (75mg TID) and ISDN 120 mg (40mg TID)

• Bidil – combo drug: – Hydralazine 37.5mg / ISDN

20mg

– 1 up to 2 tablets TID

• Adherence difficult

• Adverse Reaction – Headache

– Dizziness

– GI complaints

147

Consider slower titration to enhance

tolerance

CNEA / Key Choice

2017


Stage C Recommendations

• Digoxin can be beneficial in patients with HFrEF, unless contraindicated, to decrease hospitalizations for HF (Class IIa, LOE: B)

• (

• Improved symptoms, exercise tolerance and quality of life

• NYHA Class II-III HF treated with digoxin 2-5 years had modestly reduced combined risk of death and hospitalization

• NO EFFECT ON MORTALITY

148

How Digoxin Works

• Inhibits the NA+ and K+ membrane pump

▼

• Increase in intracellular Na+ ▼

• Enhances the Na+ and Ca++ exchange

▼

• Leads to ▲in intracellular Ca++

▼

• ▲inotropic activity (weak)

• Beneficial in heart failure

• Administration of digoxin – Improves baroreceptor

function that results in ↓ activation of the sympathetic nervous system

– ↑ vagal tone – ↓ sympathetic nerve

discharge – ↓serum norepinephrine

concentrations and plasma renin activity

149

CNEA / Key Choice

2017


• ↑ vagal activity

• ↓ conduction velocity through the AV node

• HOWEVER: Sympathetic stimulation easily overrides the inhibitory effects of digoxin on AV node conduction

• No better than placebo in converting atrial fib to Sinus Rhythm

• The conduction velocity ↑in the atria, but ↓ in the AV node.

• Automaticity is also increased, in the atria, AV node, Purkinje fibers and ventricles.

• Beta blockers are used for rate

control in HFrEF

» Addition of digoxin to BB can be

beneficial for rate control in HF

• Calcium channel blockers have

replaced digoxin as agent for rate

control in atrial arrhythmias in non

HF patients

• Digoxin remains good option in

acute setting when blood pressure

is marginal

– Give IV slowly over 5 minutes

150

Rate Control in AF Impact on Conduction

Contraindications / Cautions

• Women • Acute MI / Ischemia • Ventricular arrhythmias, Heart Block, Sick Sinus Syndrome, WPW • Hypertrophic or restrictive cardiomyopathy • Amyloid heart disease • Electrolyte abnormalities

– Hypokalemia ↑ risk of toxicity – Hypocalcemia ↓ sensitivity to digoxin – Don’t give IV calcium if digoxin toxic

151

Digoxin may be particularly beneficial in patients with a LVEF less than 25%, symptoms with minimal exertion or at rest, and/or

cardiomegaly on chest x-ray

CNEA / Key Choice

2017


• Has a narrow therapeutic range

• Toxicity may occur at therapeutic levels or lower

• Lower doses routinely used - 0.125 mg daily

– Especially if > 70 years of age, impaired renal function, or low lean body mass

• No need for loading dose in HF

• Amiodorone increases serum digoxin concentration (digoxin doses must be reduced if starting amiodarone)

• Multiple other medication interaction and will cause increased digoxin levels – assess carefully

• Dialysis is not effective with digoxin toxicity because of high tissue binding of digoxin

152 Dig Level Goal in HF: 0.5-0.9ng/mL

• EKG Changes with Toxicity – Increased automaticity with impaired conduction is common

• Re-entrant tachycardias • Paroxsysmal atrial tachycardia with AV Block • Heart block

• GI Symptoms with Toxicity – N & V (most frequent 1st sign) – Anorexia

• Neurologic Symptoms with Toxicity – Headache – Confusion – Visual disturbances: halos, change in color perception

153

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154

REMEMBER: Maximum tolerated dose is the

pharmacologic treatment goal!!!

155

Drug class Brand name

generic name Starting dose Target dose

ACE Inhibitor Prinivil or Zestril

lisinopril 5 mg once daily 20 mg once daily

maximum dose might be 40 mg once daily

ACE Inhibitor Monopril

fosinopril sodium 10 mg once daily

5 mg if weak kidneys 40 mg once daily

ACE Inhibitor Vasotec

enalapril maleate 2.5 mg BID 20 mg BID

maximum dose might be 40 mg BID

ACE Inhibitor Mavik

trandolapril one mg once daily 4 mg once daily

ACE Inhibitor Capoten captopril

25 mg 2 to 3 times a day 100mg TID (450 mg per day maximum)

ACE Inhibitor Lotensin

benazepril

5 mg once daily if on diuretic

10 mg once daily if not on diuretic

40 mg per day in one 40 mg dose or two 20 mg doses

ACE Inhibitor Accupril quinapril

5 mg BID 2.5 mg BID if weak

kidneys 20 mg BID

ACE Inhibitor Altace

ramipril 1.25 mg to 2.5 mg BID 10 mg BID

ACE Inhibitor Aceon

perindopril erbumine

1 mg BID if on diuretic 2 mg BID if not on

diuretic 4 mg BID (8 mg BID maximum)

http://www.chfpatients.com/ace.htm

http://www.chfpatients.com/text/lisinopril.txt

http://www.chfpatients.com/text/enalapril.txt



http://www.chfpatients.com/glossary.htm




http://www.chfpatients.com/ace.htm

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156

Drug class Brand name

generic name Starting dose Target dose

ARB Cozaar

losartan

25 mg BID or 50 mg once daily

12.5 mg BID or 25 mg once daily if weak

liver function

50 mg BID

ARB Atacand

candesartan cilexetil 4 to 8 mg once daily 32 mg once daily

ARB Diovan

valsartan 80 mg once daily 160 mg once daily

80 mg once daily if weak liver function

ARB Avapro

irbesartan 150 mg 300 mg once daily

Beta-blocker Coreg

carvedilol 3.125 mg BID

25 mg BID under 188 pounds

50 mg BID over 187 pounds

Beta-blocker Toprol XL

metoprolol extended release (succinate)

12.5 mg for class 3 to 4 patients

25 mg for class 1 to 2 patients

200 mg once daily

Beta-blocker Zebeta

bisoprolol 2.5 mg once daily 10 mg once daily

Aldosterone Antagonist

Aldactone spironolactone

25 mg once daily 25 mg once daily

Aldosterone Antagonist

Inspra eplerenone

25 mg once daily 50 mg once daily

Medical Therapy for Stage C HFrEF:

Magnitude of Benefit Demonstrated in RCTs

GDMT RR Reduction

in Mortality

NNT for Mortality

Reduction

(Standardized to 36 mo)

RR Reduction

in HF

Hospitalizations

ACE inhibitor or

ARB 17% 26 31%

Beta blocker 34% 9 41%

Aldosterone

antagonist 30% 6 35%

Hydralazine/nitrate 43% 7 33%

157

http://www.chfpatients.com/text/candesartan_cilexetil.txt

http://www.chfpatients.com/text/valsartan.txt

http://www.chfpatients.com/text/irbesartan.txt

http://www.chfpatients.com/beta_overview.htm



http://www.chfpatients.com/coreg.htm

http://www.chfpatients.com/CHFinfo.htm




http://www.chfpatients.com/meds_old.htm

http://www.chfpatients.com/meds.htm

CNEA / Key Choice

2017


Incremental Benefit with HF Therapies (Cumulative % Reduction in Odds of Death at 24 Months Associated with Sequential Treatments)

+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. 158

Diuretics • Decrease congestive

symptoms

– No mortality benefit

• First line: Loop diuretics – Thiazide diuretic my be added

• Potassium and magnesium monitoring

• Use with moderate NA restriction

• Fluid restriction criteria

• Monitor response to therapy

– Adequate diuresis • BNP or NT-pro BNP

goal

• JVP assessment

• Orthopnea

– Over diuresis • Hypotension

• Dizziness

• Orthostatic BP

159

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Renal Anatomy: Nephron and Loop Diuretics

160

• Work in ascending loop of Henle • Loss of H2O, K+, Na+, Cl-, H+ • More loss of H2O and less K+ and Na+ than

thiazides • Promotes venous vasodilatation • Rapid onset and short duration • Can be effective in presence of renal failure • High ceiling diuretic / threshold

medications

161

Proximal Convoluted Tubule Mannitol

Distal Convoluted Tubule Thiazide Metolazone

Thick Ascending Limb of Loop Bumetanide Furosemide Torsemide

Distal Renal Tubule Spironolactone

CNEA / Key Choice

2017


Diuretic Therapy

Outpatient

• Weight loss goal of 0.5 to 1.0 kg per day

• Patients can be educated for adjustable diuretic dosing • Weight gain

• Change in oral intake or during periods of illness

Diuretic Resistance

• Diuretic resistance – Reasons

• High sodium levels

• NSAIDs

• Severe renal impairment

• Renal hypoperfusion

– Strategies • IV instead of PO

– Continuous infusion versus intermittent dosing if BP is a concern

• Change the loop diuretic

• Addition of thiazide

• Higher dose spironalctone

162

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 renal function

163

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Loop Diuretics

• Equivalents – Furosemide 40 mg – Torsemide 20 mg – Bumetanide 1 mg

• Dosing

– Adequate to relieve symptoms

– Threshold medication – In hospital: Convert home

PO dose to IV at equal or greater than home dose

Bumetanide (Bumex)

Furosemide (Lasix)

Torsemide (Demadex)

164

Differences in Loop Diuretics

Bumetanide Furosemide Torsemide Lack of randomized control data with comparison to furosemide Better pharmacokinetic profile (oral bioavailability) than furosemide but torsemide has evidence of more efficacy and more safety Oral Bioavailability 80% Max dose 10mg / day Onset 30-60min Peak 1-2 hours Duration 4 hours May repeat every 4-5 hours

BID Dosing when GFR is low Oral Bioavailability 50% Max dose 600mg/day Onset 60min Peak 1-2 hours Duration 6-8 hours May repeat every 6-8 hours

2 randomized trials comparing Torsemide and Furosemide Torsemide associated with reduction in HF and CV readmission in systolic HF with a trend towards reduction of all cause mortality. Oral Bioavailability 80-100% Max dose 200mg/day Onset 60min Peak 1-2 hours Duration 6-8 hours May repeat every 6-8 hours 165

CNEA / Key Choice

2017


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 renal function

166

Thiazide Diuretics

– Inhibit reabsorption of Na+ and Cl-

• In the distal convoluted tubule

• More sodium loss than loop diuretics

– Delayed onset but longer duration of action than loop diuretics

• Give 30 minutes before a loop diuretic

– LOW CEILING DIURETICS

– Less potent diuretic than loop diuretics

– Diminished effectiveness in presence of renal failure 167

CNEA / Key Choice

2017


Thiazide Diuretics

Bendrofluazide (Naturetin) SIDE EFFECTS:

Blood Chemistry changes::

Hyponatremia (↓ Na+)

Hypokalemia (↓ K+)

Hypomagnesemia (↓ Mg+)

Hyperglycemia (↑ blood sugar)

Hyperuricemia (↑ uric acid)

Hypercalcemia (↑ Ca++)

Decreased glomerular filtration in

kidneys (↑ BUN, creatinine)

↑ cholesterol

↑ triglycerides

↓ HDL cholesterol

OTHER SIDE EFFECTS:

Impaired glucose tolerance

Gout

Impotence

Ventricular arrhythmias (↓ K+)

Nausea, dizziness, headache

Benthiazide (Aquatag, Exna)

Chlorothiazide (Diuril)

Chlorthalidone (Hygroton)

Cyclothiazide (Anhydron)

Hydrochlorothiazide (HCTZ) (HydroDiuril, Esidrix)

Hydroflumethazide (Saluron, Diucardin)

Indapamide (Lozol)

Metolazone (Zaroxolyn)

Polythiazide (Renese)

Trichlormethiazide (Metahydrin, Naqua)

168

Diuretics and Renal Function

• Role of venous congestion in worsening renal function

• Role of volume depletion / hypotension and worsening renal function

169

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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)

170

IMPORTANCE OF VENOUS CONGESTION FOR WORSENING OF RENAL FUNCTION IN

ADVANCED DECOMPENSATED HEART FAILURE. MULLENS ET AL. (2009). JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 53(7), 589-596.

We observed in our patient population with low-output decompensated HF that besides the presence of intrinsic renal insufficiency, venous congestion was the strongest hemodynamic determinant for the development of WRF (worsening renal failure).

In contrast, impaired Cardiac Index on admission and improvement in Cardiac Index after intensive medical therapy had a limited contribution to WRF.

171

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Increased CVP is associated with impaired renal function and independently related to all-cause mortality in a broad spectrum of patients with cardiovascular disease.

172

INCREASED CENTRAL VENOUS PRESSURE IS ASSOCIATED WITH IMPAIRED RENAL FUNCTION AND

MORTALITY IN A BROAD SPECTRUM OF PATIENTS WITH CARDIOVASCULAR DISEASE.

Damman, K. et al, (2009). Journal of the American College of Cardiology, 53(7), 582-588.

NEW KIDS ON THE BLOCK

173

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• Sinus node inhibition • Inhibition of the Hyperpolarization –activated

cyclic nucleotide-gated channels (If channel or f-channel or “Funny” channel)

• If current is an inward Na+/K+ current that activates pacemaker cells of the SA Node

• Ivabradine binds the “Funny” channel in a current dependent fashion

• Slows diastolic depolarization → slows the firing of the SA Node → slows heart rate

174

Ivabradine (Corlanor)

Impact of HR on Heart Failure

• In patients with coronary artery disease and left-ventricular dysfunction, a heart rate of 70 beats per minute (bpm) or higher was associated with a 34% increased risk of cardiovascular death and a 53% increase in admission to hospital for heart failure compared with heart rate lower than 70 bpm1

• Heart rate is also directly related to risk of death, cardiovascular death, or admission to hospital in patients with heart failure2

• Heart-rate reduction is associated with improved outcomes3

175

1. Fox K et al. on behalf of the BEAUTIFUL investigators. Heart rate as a prognostic risk factor in patients with coronary artery disease and leftventricular systolic dysfunction (BEAUTIFUL): a subgroup analysis of a randomised controlled trial. Lancet 2008; 372: 817–21

2. Pocock SJ, et al. Predictors of mortality and morbidity in patients with chronic heart failure. Eur Heart J 2006; 27: 65–75.

3. Flannery G et al. Analysis of randomized controlled trials on the effect of magnitude of heart rate reduction on clinical outcomes in patients with systolic chronic heart failure re

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2017


176

177

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• SHIFT Trial (2010) • Double-blinded, placebo-controlled, parallel-

group study • Symptomatic HF, LVEF < 35%, in NSR with HR

> 70 bmp, admitted for HF in previous year, on stable HF treatment

• 6558 patients randomized to ivabradine 7.5mg BID or matching placebo

• Primary endpoint: composite of CV death or hospital admission for worsening HF

178


• Median follow up 22.9 months • Mean HR lowered to • Statistically significant outcomes:

– Composite endpoint (CV death or Hospitalization for HF): 18% reduction with Ivabradine

– Hospitalization for worsening HF: 26% reduction with Ivabradine – Deaths due to HF: 26% reduction in Ivabradine group (CV deaths

and all cause deaths not statistically significant) – The higher the baseline heart rate the better the outcome – Quality of Life scores better with ivabradine

• Side Effect: Phosphenes (visual disturbances) reported in 3% of ivabradine group (1% in placebo – p<0.0001)

179

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2017


ACC/AHA/HFSA Guideline Update Recommendations for Ivabradine (Stage C HFrEF)


IIa B-R Ivabradine can be beneficial to reduce HF hospitalization for patients with symptomatic (NYHA class II-III), stable chronic HFrEF (LVEF < 35%) who are receiving GDEM, including beta blocker at maximum tolerated dose, and who are in NSR with a heart rate of > 70 bmp at rest.

180



181

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2017


• Nutritional supplement as treatment for HF – Coenzyme Q10

– Carnitine

– Taurine

– Antioxidants

• Hormone therapies outside correcting deficiencies – Growth hormone

– Thyroid hormone

• Antiarrhythmics

• Calcium channel blockers – Myocardial depressant

– Except amlodipine – neither harm nor benefit in HF –OK for HTN / ischemia control

• NSAIDs – Cause sodium and water

retention

• Thiazolidinediones – Associated with increase

incidence of HF 182

Cardiac Resynchronization

Therapy

183

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Cardiac Resynchronization Therapy (CRT)

• Treatment modality for heart failure not just pacing – Used in conjunction with optimal medical therapy

• Goals: – Improves contractile function – Diminishes secondary mitral regurgitation – Can reverse ventricular remodeling – Can improve LVEF – Improvement in blood pressure may allow for increased up

titration of medications – furthering increasing LV function – Improve quality of life – Decrease mortality and morbidity

184

Normal Ventricular Depolarization

185

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2017


Ventricular Depolarization with LBBB

186

Implantation of CRT

187

Where are the leads?

CNEA / Key Choice

2017


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

188

Green: Class I (Benefit >> Risk) Gold: Class IIa (Benefit > Risk) Orange: Class IIb (Benefit > Risk Red: Class III (No benefit or harm)

Indications for CRT

189

LVEF < 35% GDMT for > 3 months OR GDMT > 40 days if myocardial infarction

Expected survival > 1 year

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


LVEF <35%






implanted device



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






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



pacing (>40%)



required and rate


near 100%

ventricular pacing

with CRT

Special CRT

Indications



LVEF <35%






implanted device



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






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



pacing (>40%)



required and rate


near 100%

ventricular pacing

with CRT

Special CRT

Indications



LVEF <35%






implanted device



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






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



pacing (>40%)



required and rate


near 100%

ventricular pacing

with CRT

Special CRT

Indications



LVEF <35%






implanted device



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






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



pacing (>40%)



required and rate


near 100%

ventricular pacing

with CRT

Special CRT

Indications

CNEA / Key Choice

2017


CRT

• Causes of Loss of Bi V pacing: – Long AV Delays – Prolonged PVARP – ST with 1 degree AV Block – Lead dislodgement – Atrial fibrillation – Ventricular Ectopy

190

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.

Diuretic dose may need to be decreased after initiation of CRT.

191

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• RV pacing results in mechanical dysynchrony (mechanical LBBB)

• Similar changes occur as do with LBBB normally: – LV remodeling – Systolic dysfunction – Decreased perfusion – Wall motion abnormalities – Mitral valve regurgitation – Increased risk of AF and HF

192

Importance of Minimizing RV Pacing with DUAL Chamber Pacemakers


• Increased hospitalizations for HF (DAVID Trial)

• Increased mortality (DAVID Trial)

• No improvement in mortality, HF hospitalizations or stroke free survival when compared to VVI (MOST Trial, CTOPP Trial)

• AAI pacing demonstrates improved outcomes

• Reducing RV pacing to less than 10% in patients with dual chamber pacemakers reduced the relative risk of developing persistent atrial fibrillation by 40% compared to conventional dual chamber pacing (SAVE PACe Trial)

193

CNEA / Key Choice

2017


• Pacer Lead Placement Options – His Bundle

– RV outflow tract

– RV septal sites

– Dual pacers in RV

– LV pacing

– Biventricular pacing

• Programming Options

– DDIR mode

– AAIR mode with mode switching

– VVI mode with low rate for those being paced as defibrillation back up only

– Long AV delays

194


Automatic Implantable Cardioverter Defibrillators

Functional status / 1 year Turning off

195

CNEA / Key Choice

2017


196

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

197

CNEA / Key Choice

2017


ICD Functions

• ATP-Anti tachycardia Pacing – Tiered Antiarrhythmic Therapies

198

ICD Functions

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

wave

199

CNEA / Key Choice

2017


200

ICD Functions

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

shock for VF

Differentiate CRT-D from CRT-P

201

CNEA / Key Choice

2017


Data from ICD – Optivol Medtronic

202

Internal Monitoring with Devices

• Heart rate variability / Night heart rate

• Patient activity

• Impedance / Volume assessment

• Atria fib burden

• Ventricular arrhythmias

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

203

CNEA / Key Choice

2017


CardioMEMs CHAMPOIN Trial (2011)

• Clinical Trial Indications: Patients 18 years older with NYHA Class III heart failure for at least 3 months, irrespective of left ventricular ejection fraction and a hospitalization for heart failure within the past 3 months. Current manufacturer recommendations (post FDA approval): NYHA Class III HF hospitalized in the past year for heart failure.

• Randomized to CardioMEMS or standard treatment for heart failure. During the entire follow-up (mean 15 months [SD 7]), the treatment group had a 37% reduction in heart-failure-related hospitalization compared with the control group (158 vs 254, HR 0·63, 95% CI 0·52–0·77; p<0.0001).

• Conclusion: The addition of information regarding pulmonary artery pressure to clinical signs and symptoms improves heart failure management and reduces heart failure readmissions. Quality of life data is also available.

• Current Practice: Current practice is representative of the control group in this trial which includes monitoring signs and symptoms(reporting of symptoms and daily weights) as in the control group in the CHAMPION Trial.

• Safety: 98.6% free of device complications.

204

205

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2017


Cardiac Rehabilitation

• Centers for Medicare & Medicaid Services (CMS) determined that the evidence was sufficient to expand coverage for cardiac rehabilitation services to beneficiaries with stable, chronic heart failure – Feb. 2014 – patients with left ventricular ejection fraction of 35% or less – New York Heart Association (NYHA) class II to IV symptoms

despite being on optimal heart failure therapy for at least six weeks.

– Stable patients are defined as patients who have not had recent (≤6 weeks) or planned (≤6 months) major cardiovascular hospitalizations or procedures.

• Medicare anticipates a potential reduction of 30 day readmissions by 30% with participation in Cardiac Rehab

206

Cardiac Rehab

• The largest single trial, HF-ACTION (Heart Failure: A Controlled Trial Investigating Outcomes of Exercise Training)

• Showed a reduction in the adjusted risk for the combined endpoint of all-cause mortality or hospitalization (hazard ratio: 0.89, 95% confidence interval: 0.81 to 0.99; p = 0.03).

• Quality of life and mental depression also improved. • CHF-related counseling, whether provided in isolation

or in combination with CR exercise training, improves clinical outcomes and reduces CHF-related hospitalizations.

207

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2017


Cardiac Rehab After Advanced Therapy

• Transplanted heart lacks neural regulatory and feedback controls – Resting heart rate is high with a delayed increase with

exercise – Rate response to exercise can be erratic and unpredictable – Use of symptom-based monitoring such as the Borg scale

or other rating of perceived exertion is required.

• Blood pressure measurement in the LVAD patient requires a doppler ultrasound device – Goal between 70-90 mm Hg considered safe

• LVAD patient perceived exertion is very important since it is not clear if HR is reliable

208

ACUTE DECOMPENSATED HEART FAILURE

209

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2017


• 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.

Acute Decompensated Heart Failure (ADHF)

210

Acute Decompensated HF represents a sentinel

prognostic event.

Readmission rate predicted to be 50% at 6 months.

1-year mortality of approximately 30% of ADHF admissions

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

212

CNEA / Key Choice

2017


Hospitalization Recommended

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

213

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

214

CNEA / Key Choice

2017


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 program

215

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)

216

CNEA / Key Choice

2017


Evaluation Guides Treatment Decisions

• Determine

– Volume Status

– Perfusion Status

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

– Ejection fraction

• HFpEF

• HFrEF

217

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

218

CNEA / Key Choice

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Backwards Failure:

Pulmonary Congestion

Forwards Failure:

Hypoperfusion

219

Warm and Dry

Normal Perfusion

No Congestion

Warm and Wet

Normal Perfusion

Congestion

Cold and Dry

Low Perfusion

No Congestion

Cold and Wet

Low Perfusion

Congestion

220

CNEA / Key Choice

2017


Treatment for Acute Decompensated HF

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 221

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

222

CNEA / Key Choice

2017


223

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.

• Preload Reduction – Venous Vasodilators

• Afterload Reduction – Arterial Vasodilators

• Three Primary Drugs – NTG

• IV Primary Venous Vasodilator

– Neseritide

• Mixed

– Nitroprusside

• Predominantly Arterial Vasodilator

Vasodilator Therapy

224

There are no data that suggest that intravenous vasodilators improve outcomes in the patient hospitalized with HF

Use of intravenous vasodilators is limited to the relief of dyspnea in the hospitalized HF patient with intact blood pressure. Yancy et al, 2013.

CNEA / Key Choice

2017


A Closer Look at Venous Versus Arterial Vasodilators

• Some medications do both

• Some depend on dose • Nesiritide

• NTG

• Nitroprusside

• CA Channel blockers

• PDE Inhibitors

• ACE Inhibitors

• Other Vasodilators

225

Nitroglycerin

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

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

• Primarily used as venodilator to quickly reduce preload – Sublingual tablets provide high enough dosage to

dilate arteries and veins

226

CNEA / Key Choice

2017


Nitroglycerin

• Side Effects: – H/A, – Hypotension, – Flushing

• Caution in patients with tachycardia or bradycardia

• Caution in severe aortic stenosis or hypertrophic cardiomyopathy with obstruction

• 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

227

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

228

CNEA / Key Choice

2017



• 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

229


• Patient must have systolic BP > 90 mmHg – Longer half-life

resulting in more persistent hypothension

• 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

230

Monitor BP closely during administration.

CNEA / Key Choice

2017


Nesiritide: Where do we stand?

231

• Sackner-Bernstein et al., 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.

• 3 trials – randomized double-blind study of patients with ADHF

• 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

232

• Effect of Nesiritide in Patients with Acute Decompensated Heart Failure

• O'Connor et al. July 7 2011

• Randomized 7,141 patients

• 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.

CNEA / Key Choice

2017


2013: ROSE Trial

• Low dose dopamine and low dose nesiritide against placebo for enhance decongestion

– Neither enhanced decongestion or improved renal function

• Difference in outcome between preserved and reduced ejection fraction (Sub Study analysis 2014)

– Low dose dopamine and low dose nesiritide impacted urine output in patients with HFrEF

233

Nitroprusside • Mixed venous and arterial

dilator (primarily arterial including pulmonary bed)

• 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

234

CNEA / Key Choice

2017


If No Improvement With Preload Reduction

• Na and fluid restrict • Increase dose of loop

diuretic • Continuous infusion of

loop diuretic • Add 2nd diuretic PO

– Metalazone – Spironolactone

– OR IV chlorothiazide

• Low dose dopamine • Consider ultrafiltration

• Diuretic Resistance

– Reasons

• High sodium levels

• NSAIDs

• Severe renal impairment

• Renal hypoperfusion

235

• Ultrafiltration may be considered for patients with obvious volume overload to alleviate congestive symptoms and fluid weight (Class IIb Level of Evidence: B)

• Ultrafiltration may be considered for patients with refractory congestion not responding to medical therapy. (Class IIb Level of Evidence: C)

236

CNEA / Key Choice

2017


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.

237

• 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

238

CNEA / Key Choice

2017


Autonomic Nervous System

Sympathetic

Beta 1

HR

Contractility

Conductivity

Beta 2

Bronchodilation

Arterial Vasodilation

Alpha 1 Arterial

Vasoconstriction

Parasympathetic Vagal Response HR 239

A Closer Look at Sympathomimetics

• Sympathomimetics that increase contractility (inotropes) (β1 receptors)

– Epinephrine

– Dobutamine

– Dopamine

– Norepinephrine

240

Used primarily as

inotrope

Used primarily as

vasopressor but has

inotropic properties

when used

CNEA / Key Choice

2017


Dobutamine

241

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

Risk of ventricular arrhythmias

Synthetic Compound

Phosphodiesterase Inhibitors

• New generation: 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)

• Nursing Considerations: – Onset IV: Immediate

– Peak: 10 minutes

242

CNEA / Key Choice

2017


Phosphodiesterase Inhibitors: Non Sympathomimetic Inotropes

243

Used as an

Inotrope

BUT…..

Also has……

Preload

Reduction

Afterload

Reduction

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

244

CNEA / Key Choice

2017


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

245

Mimics endogenous dopamine;

metabolic precursor

of norepinephrine and epinephrine

Comparison of Dopamine to Norepinephrine in Shock

246

• 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.

CNEA / Key Choice

2017


247

INTRA AORTIC BALLOON PUMP

Can provide significant afterload reduction in acute decompensated heart failure

248

CNEA / Key Choice

2017


249

IABP: Counterpulsation Therapy

• Intra Aortic Balloon (IAB) is inflated during diastole and deflated during systole

• The IAB is a volume displacement device

• IAB Placement – Descending thoracic

aorta

– 1 to 2 cm below the subclavian artery origin

– Above renal and mesenteric arteries

250

CNEA / Key Choice

2017


252

Hemodynamic Impact of IAB Pumping

• Decreased systolic aortic pressure

• Decreased afterload – Decreased MVO2

• Decreased LV wall tension

• Decreased preload – Decreased pulmonary congestion

• Decreased HR

253

Indications / Contraindications

Indications • Cardiogenic shock.

• Recurrent ischemia / extending myocardial infarction.

• Unstable angina.

• Intractable ventricular dysrhythmias.

• Support for high risk intervention.

• Bridging device in acute cardiac failure.

• Mechanical defects such as acute mitral regurgitation.

• Post-operative myocardial dysfunction.

Absolute Contraindications • Aortic valve insufficiency /

regurgitation

• Dissecting aortic aneurysm

• Aortic stents

Relative Contraindications • Calcific aortic iliac disease

• Peripheral arterial disease

• Abdominal aortic aneurysm

• Thrombocytopenia

CNEA / Key Choice

2017


259

Discussion of Key Nursing Considerations

• Pressure assessment for optimization of therapy

• Balloon mobility

• Left radial pulse assessment

• Urine output

• Distal pulse assessment

• Groin care

• Platelets

• Other complications : aortic dissection

Impella • Temporary (≤ 6 hours)

ventricular support device

• Indicated for use during high risk PCI performed in elective or urgent hemodynamically stable patients with severe coronary artery disease and depressed left ventricular ejection fraction

• 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) 260

CNEA / Key Choice

2017


• Complex patient

• Monitor for limb ischemia – at least hourly

• Anticoagulation required – maintain APTT for 45-55 seconds

• Monitor for hemolysis – Decreased HGB/HCT, haptoglobin

– Hemoglobinuria may develop and AKI

– Impella Console • P8 – performance level 8 is standard with 50,000 revolutions

per minute to provide a flow rate of 1.9-2.5 L/min of cardiac output

262

Impella – Nursing Care

• Physiologic Impact – Increase forward flow

– Unloads LV

– Augments cardiac output

– Increases mean arterial pressure

• Contraindications – Mechanical aortic valve

– Moderate to severe aortic disease

– Left ventricular thrombus

– Moderate to severe peripheral arterial disease

263

Impella

CNEA / Key Choice

2017


• Venous – arterial

– allows for gas exchange and provides hemodynamic support by bypassing the lungs and heart.

– can also work alongside native circulation allowing for a portion of the blood to flow naturally through the heart and lungs.

– Indicated in refractory cardiogenic shock or as salvage strategy during cardiac arrest after 10 minutes of unsuccessful advanced cardiac life support.

264

• Venous – venous – facilitates gas exchange but does not provide for hemodynamic

support because the blood is returned to the right side of the heart before it enters pulmonary circulation.

– Pump is necessary to pump venous blood through the membrane oxygenator.

– Used as an alternative strategy in adults with ARDS to rest the lungs and avoid insult of mechanical ventilation.

• Arterial – venous – a pumpless circuit – blood flows from the femoral artery through a membrane and

returns to the femoral vein. – Hemodynamic support comes from the patient’s own cardiac

output. – Absence of a pump makes this mode easier for transport.

However, cardiac function must be well preserved.

265

CNEA / Key Choice

2017


ECMO

266

TandemHeart

• Provides 5.0 liters of cardiac output

• Augment flow of blood

• Decompress the LV

• Temporary Cardiopulmonary bypass

• Takes blood from LA to Femoral artery

267

CNEA / Key Choice

2017


268

• 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

269

CNEA / Key Choice

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ADDITIONAL CARE ISSUES

270

• 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

271

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• 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

272

• Sodium restriction is reasonable for patients with symptomatic HF to reduce congestive symptoms (IIc)

• Clinicians should consider some degree of sodium restriction (< 3 grams /day) for patients with Stage C and D HF

273

CNEA / Key Choice

2017


• 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

274

• 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.

275

CNEA / Key Choice

2017


Manage Comorbidities

• Atrial fibrillation

• Valvular Heart Disease

• Renal dysfunction

• Sleep disorder breathing

• COPD

• Hypertension

• CAD

• Peripheral artery disease

• Anemia

• Diabetes

• Obesity

• Depression and anxiety

• Cognitive dysfunction

276

Atrial Fibrillation

277

CNEA / Key Choice

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The Scope of Atrial Fibrillation in HF

♥ HF patients are more likely than the general population to develop atrial fibrillation

♥ There is a direct relationship between NYHA class and the prevalence of AF

♥ 4% in NYHA Class I

♥ 40% in NYHA Class IV

♥ Independent risk factor for the development of HF

♥ AF worsens symptoms

♥ Worsens symptoms can result in inceased ventricular response

♥ Complicates HF Care 278

Classifications

♥ Recurrent – Two or more episodes of AF

♥ Paroxysmal – Terminates spontaneously

♥ Persistent – When sustained beyond 7 days

♥ Long Standing Persistent - Greater than 12 months

♥ Permanent – Opinion based on the provider and the patient to no

longer attempt to restore NSR

279 2017

Classifications

CNEA / Key Choice

2017


Atrial Fibrillation

• Rate control first and always a priority – Strict versus lenient (RACE II study) – Metoprolol (succinate / tartrate) versus carvedilol – Avoidance of calcium channel blockers in reduced LVEF – Digoxin (at rest versus activity) – Concern with AV node ablation

• When to choose rhythm control – AFFIRM and RACE: No mortality benefit with rhythm

control – Symptom control in HF – Antiarrhythmics for rhythm control in HF

• Stroke prevention 280

Additional Rate Control Information

RACE II • Strict versus lenient rate

control

• Strict – Resting HR < 80

– Exercise < 110

• Lenient – Resting HR < 110

• No benefit of strict rate control

• Note: Study population did not include a high percentage of patients with heart failure.

281

CNEA / Key Choice

2017


New 2014 Atrial Fibrillation Guideline Update

A randomized trial suggested that a lenient (<110 bpm) rate control strategy was as effective as a strict strategy (<80 bpm) in patients with persistent/permanent AF. However, the writing committee still advocates for the latter (Class IIa), as the results of this single trial were not thought to be definitive.

282

Pharmacological Considerations in Rate Control

• Calcium channel blockers versus beta blockers – All beta blockers and only two calcium channel blockers slow

conduction through AV node – Diltiazem very effective through the AV node – Metoprolol better at rate control than carvedilol

• Pros and Cons of Digoxin

– Blood pressure effect – Heart rate control at rest versus exercise

• Pros and Cons of Amiodarone – Limiting use of other antiarrhythmics (terminal half-life elimination 40

to 55 days) – May convert the patient

CNEA / Key Choice

2017


A Closer Look at Calcium Channel Blockers

Verapamil Dihydropyridines Diltiazem

Heart Rate ▼▼

▼

AV Nodal

Conduction

▼▼

------ ▼

Contractility ▼▼

▼ ▼

Arterial

Vasodilatation

284 2017

Antiarrhythmics in Atrial Fibrillation Class Specific

Medications

Purpose of Medication Major Cardiac Side Effects

Class I A

Class I B

Class I C

Disopyramide

Procainamide

Quinidine

Not used in atrial

fibrillation

Flecainide

Propofenone

Rhythm Control

Rhythm Control

Rhythm Control

Rhythm Control

Rhythm Control

Torsade de pointes, HF

Torsade de pointes

Torsade de pointes

Ventricular tachycardia , HF,

Atrial Flutter

Ventricular tachycardia , HF,

Atrial Flutter

Class II Beta Blockers Rate Control

Class III Amiodarone

Dronedarone

Dofetilide

Ibutilide

Sotalol (Also contains beta

blocker)

Rhythm / Rate Control

Rhythm Control

Rhythm Control

Rhythm Control

Rhythm Control (also

controls rate)

Torsade de pointes (rare)

* Organ toxicity

Torsade de pointes

Torsade de pointes

Torsade de pointes

Torsade de pointes, HF, Beta

blocker side effects

Class IV Calcium Channel

Blockers

Rate Control 285

CNEA / Key Choice

2017


286

In addition to cardiac criteria; sotolol and

dofetilide are renally cleared

Defined as wall thickness exceeding 1.5 cm.

Class III Antiarrhythmics

Action

Potential

Inhibits potassium ion fluxes during phase II and III of the

action potential

Actions Directly on myocardium to delay repolarization (prolongs QT);

prolongs effective refractory period in all cardiac tissue; By

definition act only on repolarization phase and should not

impact conduction

Cautions Proarrhythmic Effects (amiodarone less)

Uses Drug dependent

Drugs Amiodarone (Pacerone, Cordorone)

Dronedarone (Multaq)

Ibutilide (Corvert)

Dofetilide (Tikosyn) – most pure class III

Sotalol (Betapace) 287

CNEA / Key Choice

2017


Class III Antiarrhythmics

Amiodarone

(ARREST

Trial)

Survival to

hospital

admission

improved

29%

Approved for life threatening refractory ventricular

arrhythmias; considered before lidocaine in pulseless VT

or V fib; considered ahead of lidocaine for stable VT with

impaired cardiac function; expanded to atrial and

ventricular arrhythmias, conversion and maintenance of

atrial fib

Use in atrial fibrillation is off label

Slows conduction in accessory pathways

Originally marketed as anti-anginal (potent vasodilator)

Relaxes smooth and cardiac muscle, reduces afterload

and preload (well tolerated in heart failure and

cardiomyoapthy)

Proarrhythmias less frequent

Is also a weak sodium channel blocker, also has effects

similar to class II and IV, also has anticholinergic properties 288

More on Amiodarone

Advantages • Efficacious

• Works on atrial and ventricular arrhythmias

• One of few antiarrhythmics tolerated in HF

• Although prolongs QT – least likely to cause torsades

• IV use short term does not lead to extra cardiac effects

Potential Disadvantages

• Although it slow

conduction over accessary pathway – may slow it more over AV node and cannot be used in patients with WPW

• Long ½ life (40 to 55 days)limits the ability to change to another agent until amiodarone is cleared

289

CNEA / Key Choice

2017


Amiodarone and Iodine

• Amiodarone is an iodinated benzofuran derivative and inorganic iodine is released when the drug is administered. This could cause complications related to thyroid function, but this is a metabolic effect and is not related to an immunologic response or iodine in radiocontrast or food (Brouse, Sara D., and Stanley M. Phillips. "Amiodarone Use in Patients with Documented Allergy to Iodine‐Containing Compounds."Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy 25.3 (2005): 429-434.).

• "Hypersensitivity reaction to amiodarone in a patient with a previous reaction to an iodinated radiocontrast agent." Annals of Pharmacotherapy 41.7-8 (2007): 1310-1314.). Their argument is based upon the “Naranjo probability scale” or algorithim and the package insert. The label of amiodarone has the following statement “Cordarone is contraindicated in patients with a known hypersensitivity to the drug or to any of its components, including iodine.”

290

Potential Extra Cardiac Effects

Pulmonary toxicity without initial

symptoms / Potentially lethal interstitial pneumonitis /

Photosensitivity

Hepatotoxicity

Corneal micro deposits Optic neuropathy / neuritis

Thyroid dysfunction: Hyper or Hypo Amiodarone partially inhibits the peripheral conversion of T4 to T3. Serum T4 and reverse T3 may be increased and T3 may be decreased.

By weight amiodarone is 37% iodine Toxic side effects increase with length of use and increased dose

CNEA / Key Choice

2017


Amiodarone Monitoring

• ECG for HR, AV block and QT interval – Monitor potassium and

magnesium

• Baseline PFTs and CXR – Annual CXR – Monitor for signs of

pulmonary toxicity (i.e. non productive cough, dyspnea)

• Semi annual LFTs • Baseline thyroid function

– Monitor for signs / symptoms of thyroid dysfunction

– Q 3 to 6 months

• Monitor for CNS effects (ataxia, tremor, dizziness, peripheral neuropathy, and delirium)

• Regular ophthalmic exams • Monitor pacing and

defibrillation thresholds if device in place

• Therapeutic level is 0.5 to 2.5 mg/L – Desethyl metabolite is active

and present in equal concentration to the parent drug.

292

293

Dronedarone (Multaq)

• Rejected by FDA 2006

• Approved by FDA 2009

• Decreases hospitalizations in atrial fibrillation

– Not permanent atrial fibrillation

• Proposed safer alternative to amiodarone in terms of extra cardiac side effects

– Iodine content

CNEA / Key Choice

2017


Dronedarone

• Similar to amiodarone without iodine component and less fat soluble

• Class III antiarrhythmic (K+ channel blocker) with effects from all four classes

• Less effective than amiodarone at maintaining sinus rhythm but also less toxic

• Elimination half-life 13-19 hours

• Has both rate and rhythm control effects but is primarily indicated for rhythm control

• May reduce incidence of stroke (mechanism uncertain)

294

Dronedarone (ATHENA)

• Approved for maintenance of sinus rhythm in patients with history of paroxysmal or persistent AF or flutter with EF > 35% who are in sinus rhythm or will be cardioverted

• Dose: 400 mg PO bid with meals (no grapefruit juice)

• Contraindicated in patients with NYHA Class IV HF or NYHA Class II-III HF with recent decompensation requiring hospitalization or referral to a specialized HF clinic – > twofold increase in mortality in HF patients

• Side Effects – GI, skin disorders

– Can prolong QTc but low risk of Torsades

– Increases serum creatinine

– Interferes with digoxin metabolism

Concern: LIVER Dysfunction: 1/2011

295

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Atrial Fibrillation 2011 Focused Update ACCF/AHA/HRS Atrial Fibrillation Guidelines

Class II A Recommendation:

Dronedarone is reasonable to decrease the need for hospitalization for cardiovascular events in patients with paroxysmal AF or after conversion of persistent AF. Dronedarone can be initiated during outpatient therapy (Level of Evidence: B)

Reduces risk of recurrent atrial fibrillation after cardioversion by 25%.

296

Class III Recommendation: Dronedarone SHOULD NOT BE ADMINISTERED to patients with class IV heart failure or patients who have had an episode of decompensated heart failure in the past 4 weeks, especially if they have depressed left ventricular function (left ventricular ejection fraction 35%)

(Level of Evidence: B)

297

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CHA2DS2VASc

• C – HF or LVEF < 35%

• H – Hypertension

• A2 – < 65 (0), 65 to 74 (1), and > 75 (2)

• D – Diabetes Mellitus

• S2 – Stroke, TIA, or Thromboembolism (2)

• VA – Vascular Disease

• Sc – Gender (Female = 1)

• http://www.mdcalc.com/cha2ds2-vasc-score-for-atrial-fibrillation-stroke-risk/

299

Anticoagulation

Nonvalvular AF patients with: 1. CHA2DS2-VASc score ≥2, oral anticoagulation

is recommended (Class I). 2. CHA2DS2-VASc score of 0, it is reasonable to

omit antithrombotic therapy (Class IIa). 3. CHA2DS2-VASc score of 1: no antithrombotic

therapy, oral anticoagulation, or aspirin (Class IIb).

4. Options for oral anticoagulation include warfarin, dabigatran, rivaroxaban, and apixaban.

300

http://www.mdcalc.com/cha2ds2-vasc-score-for-atrial-fibrillation-stroke-risk/















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Obstruction of flow at the level of the aortic valve.

301

302

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303

• Rarely needed • HR/rhythm control • ACE Inhibitors: Not in severe AS

– Development of hypotension and syncope • Nitroglycerin: With Caution

– Low dose: Impact on preload – High dose: Impact on afterload

• Beta blockers: Contraindicated in severe AS – Blocks normal adrenergic response of increased HR

304

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• Volume Management – Precarious

• Exercise – No restriction in asymptomatic mild AS – Asymptomatic patients with moderate or severe AS

• Avoid competitive sports • Evaluate tolerance to exercise per stress test

• Continuous physician follow up – Annual exams

• History and physical • Serial echocardiogram

• Endocarditis prophylaxis – 2007 AHA Guidelines

305

306

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Recommendations COR LOE Exercise testing is reasonable to assess physiological changes with exercise and to confirm the absence of symptoms in asymptomatic patients with a calcified aortic valve and an aortic velocity 4.0 m per second or greater or mean pressure gradient 40 mm Hg or higher (stage C)

IIa B

Exercise testing should not be performed in symptomatic patients with AS when the aortic velocity is 4.0 m per second or greater or mean pressure gradient is 40 mm Hg or higher (stage D)

III: Harm

B

307

Aortic Stenosis: Timing of Intervention

Recommendations COR LOE AVR is recommended with severe high-gradient AS who have symptoms by history or on exercise testing (stage D1)

I B

AVR is recommended for asymptomatic patients with severe AS (stage C2) and LVEF <50%

I B

AVR is indicated for patients with severe AS (stage C or D) when undergoing other cardiac surgery

I B

308

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Aortic Stenosis: Choice of Surgical or Transcatheter Intervention (2017 Update)

Recommendations COR LOE Surgical AR is recommended for symptomatic patients with severe AS and asymptomatic patients with severe AS who meet an indication for AVR when surgical risk is low or intermediate

I B-NR

For patients in whom TAVR or high-risk surgical AVR is being considered, members of a Heart Valve Team should collaborate closely to provide optimal patient care

I C

Surgical AVR or TAVR is recommended for symptomatic patients with severe AS and high risk for surgical AVR, depending on patient-specific procedural risks, values, and preferences.

I A

TAVR is recommended for symptomatic patients with severe AS (Stage D) and a prohibitive risk for surgical AVR who have a predicted post-TAVR survival is > 12 months

I A 309

• Balloon placed across aortic valve • Fractures calcium deposits in the leaflets • Separate fused or calcified commissures • Considered palliative in the aortic position

(Class IIB) • May be used as a bridge to surgery (Class

IIB) • All benefit gone in 6 months • Development of or increased severity of AR

• Not appropriate if AR > 2+ prior to procedure

310

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311

• Mitral valve replacement highest risk for embolization

• Warfarin for all patients

– INR goal 2.5-3.0

• Life-long ASA 75-100mg in addition to warfarin

• On-X Aortic Heart Valve

– Target INR of 1.5-2.0 (Class IIB)

• Warfarin for 3 months post op in all patients (especially MV)

• Life-long ASA 75-100mg

TAVR - Warfarin may be

reasonable for at least 3 months

- Target INR 2.5 - Clopidogrel 1st 6 months - Life-long ASA 75-100mg

312

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313

• Annulus

• Leaflets

• Chordae Tendineae

• Papillary Muscles

314

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• Remain asymptomatic for years • Most frequent

– Fatigue – Dyspnea on exertion

• Progress to include – Paroxysmal nocturnal dyspnea – Orthopnea – Palpitations from atrial fibrillation

• Initial diagnosis sometimes made with new onset AF

• Mitral valve prolapse patients early on report symptoms of tachycardia, orthostatic hypotension or panic attacks

315

• EF < 60% considered abnormal

• Surgical options include: – Mitral valve repair

– Mitral valve replacement with preservation of mitral apparatus

– Mitral valve replacement with removal of mitral apparatus

• Mortality rates in those >75 higher with mitral valve surgery than aortic valve

• Mortality rates less with repair than replacement

316

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RECOMMENDATIONS COR LOE

MV Surgery recommended for symptomatic patients with chronic severe primary MR and LVEF greater than 30%

I B

MV surgery is recommended for asymptomatic patients with chronic severe primary MR and LV dysfunction (LVEF 30% to 60% and/or left ventricular end-systolic diameter ≥40 mm

I B

MV repair is recommended in preference to MVR when surgical treatment is indicated for patients with chronic severe primary MR limited to the posterior leaflet

I B

Mitral valve repair is recommended in preference to MVR when surgical treatment is indicated for patients with chronic severe primary MR involving the anterior leaflet or both leaflets when a successful and durable repair can be accomplished

I B

Concomitant mitral valve repair or MVR is indicated in patients with chronic severe primary MR undergoing cardiac surgery for other indications

I B

317

Transcatheter MV repair may be considered for severely symptomatic patients (NYHA class III/IV) with chronic severe primary MR (stage D) who have a reasonable life expectancy but a prohibitive surgical risk because of severe comorbidities

318

video

https://www.youtube.com/watch?v=j8TIkOyAHOU

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319

• In patients at increased risk, stage A HF, the optimal blood pressure in those with hypertension should be less than 130/80 mm Hg (I)

• Patients with HFrEF and hypertension should be prescribed GDMT titrated to attain systolic blood pressure less than 130 mm Hg (I)

• Patients with HFpEF and persistent hypertension after management of volume overload should be prescribed GDMT titrated to attain systolic blood pressure less than 130 mm Hg (I) 320

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IIa B-R In patients with NYHA class II and III HF and iron deficiency (ferritin <100 ng/mL or 100 to 300 ng/mL if transferrin saturation is <20%), intravenous iron replacement might be reasonable to improve functional status and QoL

321


Yancy C, Jessup M, et al. Circulation. 2017


III No

benefit

B-R In patients with HF and anemia, erythropoietinstimulating agents should not be used to improve morbidity and mortality

322


Yancy C, Jessup M, et al. Circulation. 2017

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2017


• Apnea: cessation of breathing for greater than 10 seconds

• Hypopnea: decrease in airflow for greater than 10 seconds with a 30% reduction in oxygenation

• Apnea-Hypopnea Index: index of sleep apnea severity

• OSA: Obstructive Sleep Apnea

• CSA: Central Sleep Apnea

323

• STOP Bang

• Physical Exam – BMI . 30

– Neck circumference >17 inches (male) or > 16 (female)

– oropharyngeal exam

• Diagnosis: Polysomnogram

• Apnea-Hyponea Index – < 5 medically manage

– 5-15 – mild OSA

– 15-30 – moderate OSA

– > 30 – severe OSA

• Treatment – CPAP

– BiPAP

– Adaptive servo-ventilation

324

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325

• In patients with NYHA class II–IV HF and suspicion of sleep disordered breathing or excessive daytime sleepiness, a formal sleep assessment is reasonable (IIa)

• In patients with cardiovascular disease and obstructive sleep apnea, CPAP may be reasonable to improve sleep quality and daytime sleepiness(IIb)

• In patients with NYHA class II–IV HFrEF and central sleep apnea, adaptive servo-ventilation causes harm (III: HARM)

326

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• 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

327

• 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

328

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“Advanced”

“End-Stage”

“Refractory”

329

330

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331

• 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

332

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• 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

• History of > 1 HF hospitalization in past 6 months

• Presence of all the previous features despite “attempts to optimize” therapy, including diuretics and GDMT, unless these are poorly tolerated or contraindicated, and CRT when indicated

333

• 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

334

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• 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

335

• >2 should 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

336

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End of Life Decision Making

• Palliative Care versus Hospice

– When should they be involved

– Should be involved with all patients being considered for transplant or VAD implant

– Never to early to get them involved

• Make an assessment – Help patient and family understand the trajectory

of the disease process

• Have the discussion

337

Components of effective shared decision making include:

• 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

Allen, 2012. 338

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Palliative Care

• An approach that improves the quality of life of patients and their families facing the problem associated with life-threatening illness, through the prevention and relief of suffering by means of early identification and impeccable assessment and treatment of pain and other problems, physical, psychosocial and spiritual. (World Health Organization)

• Focuses on providing patients with relief from the symptoms and stress of a serious illness. The goal is to improve quality of life for both the patient and the family.

339

Palliative Care

• Provides relief from pain and other distressing symptoms;

• Affirms life and regards dying as a normal process;

• Intends neither to hasten or postpone death;

• Integrates the psychological and spiritual aspects of patient care;

• Offers a support system to help patients live as actively as possible until death;

• Offers a support system to help the family cope during the patients illness and in their own bereavement;

• Uses a team approach to address the needs of patients and their families, including bereavement counselling, if indicated;

• Will enhance quality of life, and may also positively influence the course of illness;

• Applicable early in the course of illness, in conjunction with other therapies that are intended to prolong life, such as chemotherapy or radiation therapy, and includes those investigations needed to better understand and manage distressing clinical complications.

• Can help decide when end of life care is appropriate 340

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Hospice Care

• Care provided to patients with a life expectancy of six months or less.

• No longer seeking a cure • Aims to make remaining time as comfortable and

as meaningful as possible. • Relief of pain • Emotional support (for patient and family) and

help with everyday tasks. • Goal: Ensure every moment counts, in the last six

months of life.

341

Continuous Inotropic Support

• Reasonable to bridge therapy in patients eligible for MCS or transplant

• Long-term, continuous intravenous inotropic support may be considered as palliative therapy for symptom control in select patients with stage D HF despite optimal GDMT and device therapy who are not eligible for either MCS or cardiac transplantation.

No mortality benefit to long term inotropic therapy. May cause harm. 342

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Home Inotropic Therapy

STAGE D HF Patients Positive IV inotropes commonly used include dopamine, dobutamine and milrinone. They are recommended for patients who: • Are unable to wean from intravenous to oral therapy • Are not likely to survive discharge without ongoing

inotropic support • Have repeatedly failed all alternative attempts to achieve

stability • Are awaiting cardiac transplant • Are receiving therapy as part of an overall plan to allow the

patient to die at home

343

• Stage D Heart Failure and acute decompensated HF not responding to treatment

• Bridge to transplant (BTT) for those who are transplant eligible

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

• Bridge to Candidacy (BTC)

• 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

344

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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

347

348

http://www.google.com/url?sa=i&rct=j&q=&esrc=s&frm=1&source=images&cd=&cad=rja&docid=bSIEXoebKJ3HeM&tbnid=AxnULaz6UEAqjM:&ved=0CAUQjRw&url=http://circ.ahajournals.org/content/126/22/2648/F1.expansion.html&ei=rrB9Ufn4GabtiwK73oC4Ag&bvm=bv.45645796,d.cGE&psig=AFQjCNESBL-9c92TLcOgSKrQkyRdnE-_bw&ust=1367278093724803

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• IABP

• ECMO

• Percutaneously implanted MCS

– Impella

– Tandem Heart

• Surgically implanted extracorporeal MCS

– CentriMag

– Thoratec pVAD II

– Abiomed BVS 5000

– Abiomed AB 5000

351

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

352

CNEA / Key Choice

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Heart Mate II

353

HeartWare HVAD

354

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Care Considerations

• Reliable social support

• Potential complications

• Patient Expectations

355

Cardiac Transplant

• Evaluation for cardiac transplantation is indicated for carefully selected patients with stage D HF despite GDMT, device, and surgical management.

• Stage D HF patients with a poor prognosis should be referred to a cardiac transplantation center for evaluation and transplant consideration

356

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Key Strategies in the Treatment of HF

EDUCATION

EDUCATION

EDUCATION 357

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.

358

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Discharge Focus 1. Diet and nutrition

2. Discharge medications

3. Activity level

4. Follow up appointments

5. Daily weight

6. Response to symptoms: Who to call

359

Hospital education should be limited to “essential” education

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”

360

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Education and Counseling

• Individualized education and counseling to focus on self care • Patients’ literacy, cognitive status, psychological state, culture, and

access to social and financial resources should be taken into account

• Treat depression and anxiety to improve education comprehension

• Repeat, repeat, repeat • Use “teach back” method

• Hospital education should be limited to “essential” education

• 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).

361

Who should be involved?

362

Identify primary care giver / support person and include

in ALL education.

CNEA / Key Choice

2017


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

363

Self-Care Behaviors

• Daily weight monitoring; avoidance of high sodium foods, taking of all prescribed medication

• Smoking cessation; avoidance of heavy alcohol intake

• Avoidance of non-steroidal anti-inflammatory drugs and other over-the-counter herbal therapies and drugs, especially decongestants and sodium-based antacids

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

• Activity and exercise: easy warm up/cool down; getting started; when to stop or slow down

364

CNEA / Key Choice

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Barriers to Self-Care Management

• 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

365

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)

• Importance of provider follow up and ongoing monitoring

• Why drugs are used in HF; how they improve survival or reduce symptoms; Understanding reason for uptitration; how to take medications for greatest effectiveness; common adverse effects

367

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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”

368

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 Importance of not running out of their medication (refill verifications with pharmacy) Regular follow-up with provider to monitor labs

369

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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 370

Daily Weights

• Use same scale, same amount of clothing

• Empty bladder and before breakfast

• Record!!

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

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

• Barriers: Confusion fluid gain from over eating gain

• Use of device data

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

• Special considerations with ECF – concern for weight loss 371

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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?

372

Diet and Nutrition

Moderate sodium restriction

Exact amount is not known

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

373

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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.

374

Low Sodium Tips

• Dining at restaurants or in another person’s home • Reading labels

– Per SERVING • Percent sodium (or) • mg sodium per serving

• 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!! 375

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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 (2L)

– - Sodium < 125 mEq (< 2L)

• Explain the thirst mechanism 376

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 systolic HF or diagnosis of stable

angina

– Consider pulmonary rehab if co-existing COPD

– 30 minutes moderate activity / exercise 5 days per week

• Work if at all possible 377

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Follow Up

• Contact within 48-72 hours from discharge

• Appointment within on week from discharge

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

• Enrollment in a HF Clinic • Allows for up titration of medications

• Continues evaluation for progression of disease – Need for ICD

– Need for CRT

– Referral for advanced therapies

– End of life planning

378

IS THERE ONE CORRECT ANSWER?

379

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Readmission Data

• 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

380

What We Know • 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

– Value of PCP f/u unclear – probably ; 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

381

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• 60% due to poor adherence to dietary and pharmacologic regimins

• Worsening cardiac function

• Arrhythmias – new onset atrial fibrillation or recurrence

– VT,VF

• CAD

• Adverse effects of cardiac medications

• Patient not adequately decongested before discharge

• Discharge regimen not adequately established – Transition from IV to PO diuretic

Readmission Reasons

382

High Risk for Readmission

• AGE/Ethnicity/Gender – >75 years

– African Americans

– Males

• Comorbid conditions – A Fib

– CAD

– HPTN

– DM

– Lung Disease

• Hemodynamics

• Previous admission ED visits

• Hyponatremia

• Anemia

• Elevated BNP

• Elevated Troponin –T


• Elevated Cystatin Level

• Depression

• Limited Health Literacy

• Low socioeconomic status

• Lack of family support

• Low patient engagement 383

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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

384

Consider

• BNP Level at discharge compared to admission

• Ambulation to assess functional class

• Orthostatic blood pressure evaluation

• Off IV medications at least 24 hours

• Off inotropes at least 24 hours

• Referrals made

• Education complete

385

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Role of Technology

• Home weight monitoring system

• Device monitoring

• CardioMEMS

386

Transitional Care

• Actions designed to ensure coordination and continuity of health care when patients move from one level to the next

• Lapses

– Absent or limited clinical information

– Lack of care plan content

– Errors related to medications

387

CNEA / Key Choice

2017


Successful Transitional Care

• Risk vs benefit of transfer evaluated • Appropriateness of new care setting determine

the transfer decision • Communication between sending and receiving

provider • Preparation of patient and care giver • Follow up plan

– Tests – Appointments – Medications

388

Transitional Care Interventions

• Systematic review 47 trails • At 30 days a high intensity home-visiting program reduced

all cause readmissions and death • At 3-6 months home-visiting programs and

multidisciplinary heart failure clinic (MDS-HF) interventions reduced all cause readmissions. (not STS or telemonitoring)

• 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 (non structured) and primarily educational interventions are not efficacious for reducing readmissions or mortality

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.

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Quality Improvement

• Process of purposeful change toward meeting accepted quality standards

• Must have indicators to evaluate success

• Clinical Practice Guidelines provide

• Outcomes

– Structure

– Process

– Outcomes

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Quality

Structure

• Relate to organizational structure and delivery of care

• Phone support

• Documentation tools – HER

Process

• Measures how recommended care is provided

• Core measures

• Correct Beta blocker order

• Documentation of discharge instructions

• Documentation of LV function

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Outcome Indicators

• Mortality

• LOS

• Readmission

• Cost

• Quality of life

• Functional class

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Accreditation Agencies

• Joint Commission Certification

• Society of Cardiovascular Care (previously Society of Chest Pain Centers)

• Healthcare Accreditation Colloquium

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396

You are caring for a patient admitted with acute decompensated heart failure. Physical assessment reveals orthopnea, elevated neck veins, crackles throughout both lungs, skin is warm and

diaphoretic. BP is 140/80, HR 96, RR 28. Which of the following drugs do you anticipate administering:

A. IV furosemide and a dobutamine infusion.

B. Hydrochlorothiazide and a dopamine infusion.

C. IV furosemide and a nitroglycerine infusion.

D. Dobutamine infusion and a nitroprusside infusion.

397

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A positive hepatojugular reflux test refers to:

A. Elevation of neck veins when pressure is applied to the sternum in right ventricular failure.

B. Elevation of neck veins when firm pressure is applied over the liver in right ventricular failure.

C. Regurgitation of liver contents into the neck veins.

D. Regurgitation of stomach contents into the esophagus in liver failure.

398

Your patient presents with acute respiratory distress, crackles half way up bilaterally, elevated neck veins, and cool

extremities with weak peripheral pulses. You assess his peripheral perfusion and pulmonary congestion status to be:

A. Congestion, peripheral hypoperfusion.

B. Congestion, normal perfusion.

C. No congestion, normal perfusion.

D. No congestion, peripheral hypoperfusion.

399

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Drugs with a positive mortality benefit in heart failure include:

A. Dobutamine, milrinone. Diuretics, calcium channel blockers.

B. Calcium channel blockers, digoxin, beta blockers, ACE inhibitors.

C. Digoxin, diuretics, beta blockers, calcium channel blockers.

D. Beta blockers, ACE inhibitors, ARBs, aldosterone blockers.

400

Which type of diuretic is the first line choice for managing heart failure:

A. Thiazide Diuretic

B. Loop Diuretic

C. Potassium sparing diuretic

D. Combination loop and thiazide diuretic

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The following are signs and symptoms specific to right sided heart failure:

A. JVD, hepatojugular reflux, cough.

B. JVD, engorged liver, crackles.

C. JVD, hepatojugular reflux, gut edema.

D. Crackles, cough, orthopnea.

402

Which of the following describes systolic dysfunction or HFrEF:

A. Ejection fraction of 60% with clear lungs.

B. Thin walled, dilated left ventricle, ejection fraction 35%.

C. Thick ventricular walls, normal LV cavity size, ejection fraction 50%.

D. Impaired relaxation of the LV with reduced LV filling.

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The most common cause of right ventricular failure is:

A. Right ventricular myocardial infarction

B. Pulmonary embolism

C. Pulmonary hypertension

D. Left ventricular failure

404

Compensatory mechanisms in heart failure that contribute to the symptoms and to the progression of

heart failure include:

A. Sympathetic nervous system and renin-angiotensin-aldosterone system stimulation.

B. Natriuretic peptides.

C. Prostaglandins and brain natriuretic peptide (BNP).

D. Nitric oxide and bradykinin.

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Your outpatient patient being managed for chronic heart failure on routine lab draw has a potassium of 5.5. The rest of his basic metabolic panel is normal.

What should you consider?

A. Admit him to the hospital for management

B. Redraw the level assuming this is a lab error

C. Have him take Kayexalate to bring the potassium down

D. Ask him to stop his aldosterone antagonist then repeat level in 3 to 5 days.

406

Diastolic heart failure, or HFpEF, is best defined as:

A. Impaired ability of the left ventricle to relax and fill.

B. Impaired ability of the left ventricle to contract and effectively eject blood.

C. Heart failure with an elevated diastolic blood pressure.

D. Heart failure in which diastole is shortened.

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When caring for a patient with chronic heart failure the nurse recognizes that the following may predispose the

patient to the development of hyperkalemia:

A. ACE Inhibitors

B. Aldosterone antagonists

C. Salt Substitutes

D. Beta Blockers

E. A, B, and C

F. All of the above

408

Orthopnea can be very suggestive of heart failure. Orthopnea is defined as:

A. Sudden onset of shortness of breath that wakes the patient from sleep.

B. Shortness of breath that occurs in a recumbent position.

C. Shortness of breath that occurs upon standing.

D. Shortness of breath that occurs with ambulation.

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All of the following describe orthopnea EXCEPT:

A. The patient sleeps in a recliner.

B. The patient uses two or more pillows to sleep at night.

C. The patient is able to fall asleep lying flat but wakes up suddenly short of breath after several hours of sleep.

D. The patient has a hospital bed and sleeps with the head elevated. 410

When assessing volume overload status in the heart failure patient, you know that a 1 kg (2.2 pounds)

weight gain is equal to:

A. 2200 ml of retained fluid.

B. 1500 ml of retained fluid

C. 1000ml of retained fluid

D. 500 ml of retained fluid

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Your 82 year old patient with a history of heart failure tells you that he is experiencing shortness of breath with his morning routine and finding it harder and harder to get dressed in the morning due to the dyspnea and fatigue. He reports he is fine when sitting in the chair

but walking across the room is becoming difficult due to the shortness of breath. This patients New York Heart Association

(NYHA) Functional Class would be:

A. NYHA Class I

B. NYHA Class II

C. NYHA Class III

D. NYHA Class IV

412

59 year old with heart failure has received diuresis while in the hospital. He is ready to be discharged. When you walked with him in

the hallway after breakfast he tells you that his breathing is much better. He was able to get washed up without difficulty. He thinks he is much better then when had came in and could hardly breath just sitting in a chair. His New York Heart Association (NYHA) Functional

Class today would be:

A. NYHA Class I

B. NYHA Class II

C. NYHA Class III

D. NYHA Class IV

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Signs and symptoms of abdominal edema and possible liver engorgement in the heart failure

patient include all of the following EXCEPT:

A. Early satiety

B. Abdominal bloating

C. Diarrhea

D. Nausea / Vomiting

414

The ACC (American College of Cardiology) and AHA (American Heart Association) guidelines for heart failure stage heart failure from stage A through D. Your patient has been admitted with heart failure. This

is a new diagnosis for the patient who has been identified a heart failure with reduced ejection fraction. Which ACC / AHA Stage of HF

would be the correct stage for this patient.

A. Stage A

B. Stage B

C. Stage C

D. Stage D

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When educating patients with heart failure about weighing themselves daily the best explanation as to why

the patient should participate in this activity would be:

A. Weighing yourself daily is a good practice of general health.

B. It is important that you eat well and maintain healthy nutrition. By monitoring your weight we can assure you are eating properly.

C. Monitoring your weight daily can identify timely changes in your weight. These weight changes alert us to possible changes in your fluid levels that may need to be addressed.

D. An increase in your weight can alert us that you are eating too much. Rapid weight changes can put more stress on your heart.

416

When a patient is identified as non-adherent to treatment the first thing the provider should do

is : A. Talk with the patient and try

to understand what the barriers are that keep the patient from participating in that aspect of care.

B. Explain to the patient why the therapy is important.

C. Be firm with the patient and tell the patient that if they do not comply they will need to find a new provider.

D. Talk to the spouse or significant other privately to identify a plan to coerce the patient into complying with the therapy. 417

CNEA / Key Choice

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Which of the following statements might make you think your heart failure patient may be moving from

the Palliative level of care to the Hospice level of care?

A. Since I was diagnosed with heart failure I knew it would kill me one day. I'm not sure what day that will be, but I'm not ready for it to be today.

B. I'll go back to the hospital but I'm staying there until they get it right this time.

C. I'm tired of going back to the hospital. Isn't there a way to treat this without repeated trips to the hospital?

D. I am not going back to the hospital. I don't want to do this anymore. I'm tired of fighting this battle. 418

Which of the following is NOT a sign of advancing heart failure?

A. Persistent hypotension

B. Persistent atrial fibrillation with high heart rates.

C. Multiple hospital admissions for heart failure

D. Worsening renal function

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You are caring for a patient whose creatinine today is 1.7 mg/dL. Yesterday the creatinine was 1.01 mg/dL. Blood pressure is 126/80 mmHg and HR is 74. What

ordered medications should be held and clarified with the provider:

A. Metoprolol succinate

B. Amiodarone

C. Lisinopril

D. Warfarin

420

Thought They may forget your

name, but they will never

forget how you made

them feel.

-Maya Angelou 421

CNEA / Key Choice

2017


Our Vision:

Practice with Joy. Positively impact every patient and family on their journey; provide safe passage; meet them where they are; connect with them in a meaningful way; and delivering care with wisdom and intention.

- Cindy and Karen

422 2017

423

BE THE BEST THAT YOU CAN BE

EVERY DAY. YOUR PATIENTS ARE

COUNTING ON IT!

Contact us: www.cardionursing.com

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