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Heart Failure



Amanda Ryan, D.O.

Cardiology Fellow

February 14th, 2008

Learning Objectives



 Following this presentation, the

participant should be able to:

 1. Recognize the magnitude of heart failure epidemic and its public

health implications

 2. Distinguish the different classifications and stages of heart failure

 3. Review underlying pathophysiology of heart failure

 4. Discuss signs and symptoms of heart failure exacerbation

 5. Identify current practice guidelines for treatment of acute

decompensated heart failure

What is Heart Failure

 Heart failure occurs when the heart cannot

pump enough blood fast enough to meet the

metabolic needs of the body.

 No longer use the term “congestive” because

all heart failure does not result in clinically

apparent volume overload

It is an Epidemic

 Estimated that over 5 million Americans have heart

failure

 Estimated 500,000 new cases per year

 Within 5 years, half of those diagnosed will be dead

 Over 1 million hospitalizations per year with HF as

primary diagnosis

 Most common reason for hospitalization in those >65

years old

 85% of HF cases are in adults 65 and older

 Heart failure is 4th in a list of quality of care initiatives in

vulnerable older adults

Costs of Heart Failure

 It is the leading cause of hospitalization in patients older than 65 years

of age and is a primary hospital discharge diagnosis in 1.1 million

people of all ages each year.

 It is one medical condition for which mortality continues to increase.

From 1994 to 2004, the overall death rate declined 2.0% in the United

States, but deaths from HF increased 28% in the same time period.

 According to the National Heart, Lung, and Blood Institute, the

estimated direct and indirect costs associated with HF care in the US is

$33.2 billion yearly.

 The majority of the costs – approximately two-thirds – are attributable

to the management of episodes of acute HF decompensation (i.e.,

hospitalization).

REACH Trial

 Researchers at Henry Ford Heart and

Vascular Institute found that the annual

number of heart failure cases more than

doubled for Henry Ford Health System in

Detroit from 1989-1997. Over that nine-year

period, 26,442 cases were identified.

Strikingly, the annual prevalence rose from 9

to 20 cases per 1000 health system patients .

Our Aging Population

Different Ways to Define HF

 Dilated (congestive) cardiomyopathy is a group of heart muscle

disorders in which the ventricles enlarge but are not able to pump

enough blood for the body's needs, resulting in heart failure.

(Example - CAD, myocarditis, EtOH, HIV)

 Hypertrophic cardiomyopathy includes a group of heart disorders

in which the walls of the ventricles thicken (hypertrophy) and

become stiff, even though the workload of the heart is not

increased. (Example – congenital HOCM, or acquired)

 Restrictive (infiltrative) cardiomyopathy includes a group of heart

disorders in which the walls of the ventricles become stiff, but not

necessarily thickened, and resist normal filling with blood

between heartbeats. (Example – radiation, amyloidosis)

Different Ways to Define HF

 Diastolic Versus Systolic Heart Failure

A. Systolic cardiac (heart) dysfunction (or systolic

heart failure) occurs when the heart muscle doesn't

contract with enough force, so there is not enough

oxygen-rich blood to be pumped throughout the

body.

B. Diastolic cardiac dysfunction (or diastolic heart

failure) occurs when the heart contracts normally,

but the ventricle doesn't relax properly so less

blood can enter the heart.

Different Ways to Define HF

 Clinically, patients are classified as having

HF of ischemic or nonischemic etiology

based on a history of myocardial infarction

(MI) or based on objective evidence of

coronary artery disease (CAD) such as

angiography or functional testing.

Controversial Definitions

Staging of Heart Failure

New York Heart Association



 Class I: No obvious symptoms, no limitations on patient

physical activity (35 percent).



 Class II: Some symptoms during or after normal activity,

mild physical activity limitations (35 percent).



 Class III: Symptoms with mild exertion, moderate to

significant physical activity limitations (25 percent).



 Class IV: Significant symptoms at rest, severe to total

physical activity limitations (5 percent).

Causes of Heart Failure

 Coronary artery disease

 Problems with the heart muscle itself [known as

cardiomyopathy (myocarditis, etc)]

 Hypertension

 Problems with any of the heart valves

 Abnormal heart rhythms (also called arrhythmias)

 Toxic substances (EtOH, cocaine)

 Congenital heart disease

 Diabetes

 Thyroid problems

 HIV

Diastolic HF

 Diastolic heart failure is defined as a condition caused by increased resistance

to the filling of one or both ventricles; this leads to symptoms of congestion from

the inappropriate upward shift of the diastolic pressure-volume relation.

k 40% of patients

k Increasing incidence with age

k More common in women

k HTN and cardiac ischemia are most common causes

k Common precipitating factors include volume overload; tachycardia; exercise;

hypertension; ischemia; systemic stressors (e.g., anemia, fever, infection,

thyrotoxicosis); arrhythmia (e.g., atrial fibrillation, atrioventricular nodal block);

increased salt intake; and use of nonsteroidal anti-inflammatory drugs.

More About Diastolic

Dysfunction

 Alterations involve relaxation and/or

filling and/or distensibility.

 Arterial hypertension associated to LV

concentric remodelling is the main

determinant of DD but several other

cardiac diseases, including myocardial

ischemia, and extra-cardiac pathologies

also possible.

Stages of Diastole

 1. Isovolumetric relaxation, period occurring between the end

of LV systolic ejection (= aortic valve closure) and the opening of

the mitral valve, when LV pressure keeps going its rapid fall while

LV volume remains constant.

 2. LV rapid filling, which begins when LV pressure falls below

left atrial pressure and the mitral valve opens. During this period

the blood has an acceleration which achieves a maximal velocity,

direct related to the magnitude of atrio-ventricular pressure, and

stops when this gradient ends.

 3. diastasis, when left atrial and LV pressures are almost equal

and LV filling is essentially maintained by the flow coming from

pulmonary veins – with left atrium representing a passive conduit

– with an amount depending of LV pressure, function of LV

"compliance".

 4. atrial systole, which corresponds to left atrial contraction and

ends at the mitral valve closure. This period is mainly influenced

by LV compliance, but depends also by the pericardial resistance,

by the atrial force and by the atrio-ventricular synchronicity (=

ECG PR interval).

Patient Differences



 HF is a hemodynamic disorder but there is a

poor relationship between measures of

cardiac performance and patient symptoms

 For example, pts with very low EF may be

asymptomatic while someone with preserved

EF may be severely disabled with symptoms

Body Compensatory

Mechanisms

 Epinephrine and norepinephrine release which increases heart rate

and contractility which increased myocardial work load

 Decrease salt and water excretion from kidneys which helps maintain

BP by increasing blood volume, this leads to stretching of heart’s

chambers which can impair ability to contract

 Hypertrophy and thickening of heart muscle which initially increases

contractility but over time leads to stiff chambers and can impair

contractility

 HF patients have higher levels of epinephrine, norepinephrine,

aldosterone, angiotensin II, endothelin, inflammatory cytokines, and

vasopressin which contribute to heart remodeling, progression of HF,

and higher levels are associated with increased mortality

Potential Reasons

 Alternation in ventricular distensibility

 Valvular regurgitation

 Pericardial restraint

 Cardiac rhythm

 Conduction abnormalities

 RV function

 Also several non-cardiac factors including peripheral

vascular fxn, reflex autonomic activity, renal sodium

handling, etc.

HF Risk Factors - History

o Smoking o Cardiotoxic drugs

o EtOH use o Fam Hx of sudden

o DM death, CAD, conduction

o HTN problems, HCM

o Dyslipidemia o HIV status

o Thyroid disorder

o Chemotherapy

o Radiation

Cardiovascular Medical Hx

p Hx of heart failure p Embolic events

p Angina p arrhythmias

p MI p CVA

p CABG p PVD

p PCI p Rheumatic Dx

p Pacemaker/ICD p Other valvular hx

p Congenital

Signs and Symptoms of HF

 Dyspnea  Rales

 PND  S3

 Orthopnea  Pulmonary edema

 Cough  JVD

 Exercise intolerance  Tachycardia

 Edema  Cardiomegaly

 Fatigue  Hepatojugular reflex

 Nausea  Peripheral Edema

 Abdominal Fullness  Hepatomegaly

HF Diagnosis and Assessment

 Remains primarily a clinical diagnosis but

additional information via other diagnostics

can be beneficial

 Evaluation depends on if this is first

presentation, change in clinical symptoms,

certainty of diagnosis, etc

Examples

 Elevated BNP levels have been associated

with reduced LVEF, LVH, elevated LV filling

pressures, and acute MI

 Evidence supports baseline levels for acute

exacerbations at this time

 Evaluation with coronary angiography on

initial dx or presentation is recommended

TTE Recommendations in Heart

Failure

ADHERE

 The Acute Decompensated Heart Failure National Registry

(ADHERE) is the largest clinical database of patients with acute

decompensated heart failure (ADHF). It provides a cross-

sectional evaluation of the HF population in the United States

and provides insights into how patients with ADHF are managed

during hospitalization.

ADHERE DATA

 The data gathered for this registry include demographic

information, medical history, baseline clinical characteristics,

initial evaluation, treatment received, procedures performed,

hospital course, and patient disposition.

 Importantly, registry participation does not require any alteration

of treatment or hospital care, and entry of data into the registry is

not contingent on the use of any particular therapeutic agent or

treatment regimen

Lessons From ADHERE

 Prior studies on chronic systolic HF have demonstrated that body mass index

(BMI) is inversely associated with mortality, the so-called obesity paradox.

ADHERE investigators sought to determine whether BMI influences the mortality

risk in ADHF, a subject not previously studied. In the large ADHERE cohort of

hospitalized patients with HF, higher BMI was associated with significantly lower

in-hospital mortality risk. The authors noted that the relationship between BMI

and adverse outcomes in HF appears to be complex and deserving of further

study.

 Since most ADHF patients present for hospital care via the emergency

department (ED), the ADHERE investigators studied the impact of early ED

initiation of ADHF-specific therapy, as indicated by nesiritide use, on subsequent

outcomes. Nesiritide was started in the ED in 1,613 patients (EDN group) and

after admission to an in-patient unit in 2,687 patients (INN group). Nesiritide was

initiated a median of 2.8 and 15.5 hours after presentation in EDN and INN

patients, respectively (p 120 ms. This electrocardiographic representation

of abnormal cardiac conduction has been used to identify patients with

dyssynchronous ventricular contraction. While imperfect, the ACC/AHA

guidelines acknowledge that no other consensus definition of cardiac

dyssynchrony exists as yet, although several echocardiographic measures

appear promising.



The mechanical consequences of dyssynchrony include suboptimal ventricular

filling, a reduction in LV dP/dt (rate of rise of ventricular contractile force or

pressure), prolonged duration (and therefore greater severity) of mitral

regurgitation, and paradoxical septal wall motion. Ventricular dyssynchrony is

associated with increased mortality in HF patients.

Evidence for CRT

 In a meta-analysis of several CRT trials, HF

hospitalizations were reduced by 32% and

all-cause mortality by 25%. The effect on

mortality in this meta-analysis became

apparent after approximately 3 months of

therapy.

Guidelines for CRT

ICD Support

 Evidence that ICDs save lives comes from

trials such as MADIT II, DEFINITE, and SCD-

HeFT

Ventricular Assist Devices

 A VAD is a temporary life-sustaining device. VADs

can replace the left ventricle (LVAD), the right

ventricle (RVAD), or both ventricles (BIVAD). They

are used when the heart muscle is damaged and

needs to rest in order to heal or when blood flow

from the heart is inadequate. VADs can also be

used as a bridge in patients awaiting heart

transplantation or in patients who have rejected a

transplanted heart.

Inpatient Vs Outpatient

Management

 Nesiritide is a new drug that is a synthetic

BNP that vasodilates vessels and serves as a

potent diuretic agent

 Inotropic agents (dobutamine, milrinone) –

often used inpt, potent inotropic agents used

to increase cardiac output – use is

controversial in outpt settings, may improve

morbidity, definite use in hospice setting,

increase risk of arrhythmias which is

important in those with AICD’s

Definition of Stage Usual Therapies



Stage

Stage A Those at high risk for developing heart

failure. Includes people with:

•Hypertension •Exercise regularly

•Diabetes mellitus •Quit smoking

•Coronary artery disease (including heart •Treat hypertension

attack) •Treat lipid disorders

•History of cardiotoxic drug therapy •Discourage alcohol or illicit drug use

•History of alcohol abuse •If previous heart attack or current diabetes mellitus or

•History of rheumatic fever hypertension  angiotensin converting enzyme inhibitor

•Family history of cardiomyopathy. (ACE-I)



Stage B Those diagnosed with “systolic” heart

failure but have never had symptoms of

heart failure (usually by finding an ejection •Care measures in Stage A +

fraction of less than 40% on •All patients should be on ACE-I

echocardiogram). •Beta-blockers should be added

•Surgical consultation for coronary artery revascularization

and valve repair/replacement (as appropriate)

Stage C Patients with known heart failure with In this group, care measures from Stage A apply, ACE-I and

current or prior symptoms. beta-blockers should be used +

Symptoms include: •Diuretics (water pills)

•Shortness of breath •Digoxin

•Fatigue •Dietary sodium (salt) restriction

•Reduced exercise intolerance. •Weight monitoring

•Fluid restriction (as appropriate)

•Withdrawal of drugs that worsen the condition

•Spironolactone when symptoms remain severe with other

therapies

Stage D Presence of advanced symptoms, after All therapies under Stages A, B and C + evaluation for:

assuring optimized medical care •Cardiac transplantation

•Ventricular assist devices

•Surgical options

•Research therapies

•Continuous intravenous inotropic infusions

•End-of-life care

Major Outcome Measurements

1. Accuracy of diagnostic instruments

2. Survival

3. Quality of life

4. Symptoms of heart failure

5. Exercise tolerance and functional capacity

6. Effects of medications to treat systolic HF on

morbidity and mortality

7. Adverse effects of drugs

8. LVEF per echo or radionuclide

9. Hospitalization rate

Health System HF Intervention

Goals

 Ensure medical management for HF is

consistent with national guidelines

 Provide residents with essential information

for self-care

 Prevent avoidable hospital readmissions

 Reduce financial burden to health care

system through clinically appropriate

utilization of resources and length of stay

 Administer preventive vaccinations

Interdisciplinary Interventions

 Implementation of protocol for heart failure in

the long-term care setting has been proven to

standardize management and strengthen the

continuum of care

 Nursing facility in Michigan which consisted

of 150 nursing home beds designed such a

program

Protocol

 Medical director, director of nursing, key

nursing unit leaders developed

 Nursing staff then received education

regarding specifics of protocol

 Admission personnel play an important role

by early recognition and requesting certain

documentation from d/c hospitals

 Recent weight and immunization hx obtained

Protocol continued

 Diagnosis verification by reviewing records,

admission Chest X-ray, echo reports, medication

review.

 Pharmacists were utilized when appropriate



 Weight monitoring program established (three times

weekly) and if more than 2 lb gain, a standard

nursing assessment

a. Included physical exam and history is possible

focusing on shortness of breath, fatigue, night

cough, LE edema, cough, change in vital signs

More Protocol

 Preventive vaccination policy

 Patient education – heart failure booklet,

family counseling when appropriate, input

from dietary and nursing staff

Quality Assurance via CMS HF

Standards

 Current echo report

 Use of ACE-I where appropriate

 Standardized nursing assessments

 Effective tx for heart failure symptoms

 90% immunization rate

 Education for resident and families for HF

Results – Echo documented

Ejection Fractions

More Results – Symptom

Management

Results – ACE-I utilization

Hospital Readmissions

 Of 22 noted clinical deteriorations at 5

months, only one resulted in a hospital

readmission in this study.

 The other declines or changes in status were

managed in the facility with early, aggressive

interventions

 Required several training sessions with

nurses, educating attending physicians, and

the involvement of facility administrator

End of Life Care

 Realization that heart failure is often a terminal

disease and while we have made great strides in

treatment, there often comes a point where the

focus of care changes to a palliative focus

 May include shutting off defibrillator

 Symptom relief, psychosocial and spiritual

considerations are of key importance

 End-of-life predominating symptoms are often

dyspnea, dry mouth, nausea, fatigue, pain,

restlessness, and apprehension.

Final Reminder – Continue to

Break Barriers

 Nursing staff, mid-level practitioners,

physicians, dietary staff, therapist, patients &

families, and other ancillary staff must realize

that together we can make the greatest

difference in treating heart failure

 HF is an epidemic with primary care staff

having the greatest potential impact by early

realization of decline and appropriate

intervention &/or referral

Citations

 Douglas et al. Appropriateness criteria for echocardiography. J Am Coll Cardiol 2007

 Poole-Wilson PA, Swedberg K, Cleland JGF, et al. Comparison of carvedilol and metoprolol on clinical

outcomes in patients with chronic heart failure in the Carvedilol Or Metoprolol European Trial (COMET):

randomized controlled trial. Lancet 2003;362:7-13.

 Remme WJ, Torp-Pedersen C, Cleland JGF, et al. Carvedilol protects better against vascular events than

metoprolol in heart failure – Results from COMET. J Am Coll Cardiol 2007;49:963-71.

 Rosamond W, Flegal K, Friday G, et al. Heart disease and stroke statistics--2007 update: a report from

the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation

2007;115:e69-171.

 Adams Jr. KF, Fonarow GC, Emerman CL, et al. Characteristics and outcomes of patients hospitalized

for heart failure in the United Statesrationale, design, and preliminary observations from the first 100,000

cases in the Acute Decompensated Failure National Registry (ADHERE). Am Heart J 2005;149:209-216.

 Higgins SL, Hummel JD, Niazi IK, et al. Cardiac resynchronization therapy for the treatment of heart

failure in patients with intraventricular conduction delay and malignant ventricular tachyarrhythmias.

JACC 2003;42:1454-1459

Citations Continued

 Peacock WF 4th, Fonarow GC, Emerman CL, Mills RM, Wynne J; ADHERE Scientific Advisory

Committee and Investigators; Adhere Study Group. Impact of early initiation of intravenous therapy for

acute decompensated heart failure on outcomes in ADHERE. Cardiology 2007;107:44-51.

 Galvao M, Kalman J, DeMarco T, et al. Gender differences in in-hospital management and outcomes in

patients with decompensated heart failure: analysis from the Acute Decompensated Heart Failure

National Registry (ADHERE). J Card Fail 2006;12:100-7.

 Fonarow GC, Peacock WF, Phillips CO, et al. Admission B-Type Natriuretic Peptide Levels and In-

Hospital Mortality in Acute Decompensated Heart Failure. J Am Coll Cardiol 2007;49:1943-50

 Hunt SA American College of Cardiology; American Heart Association Task Force on Practice Guidelines

(Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure).

ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult:

a report of the American College of Cardiology/American Heart Association Task Force on Practice

Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of

Heart Failure). JACC 2005;46:e1-e82

 Abraham WT, Fisher WG, Smith AL, et al. Cardiac resynchronization in chronic heart failure. N Engl J

Med 2002;346:1845-1853



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