heart failure by nancy jenkins the most common reason for hospitalization in adults >65 years...

HEART FAILUREby Nancy Jenkins

The most common reason for hospitalization in adults >65 years old.

Heart Failure Click here!

Heart FailureHeart Failure-- Clinical syndrome Clinical syndrome that can result from any structural that can result from any structural or functional cardiac disorder that or functional cardiac disorder that impairs ability of ventricle to fill impairs ability of ventricle to fill with or eject bloodwith or eject blood

5 million Americans have heart failure •500,000 new cases every year• 25-50 billion dollars a year to care for people with Heart Failure••6,500,000 hospital days / year6,500,000 hospital days / year••300,000 deaths/year300,000 deaths/year

MildMild

Fluid Restriction

Heart Failure

Uncompensated Heart FailurePulmonary Edema-ADHF Severe End Stage

Cardiogenic shockCardiomyopathy

Irreversible

Needs new ventricle

VADIABPVADIABP

Heart Transplant

Control With

/Same as Mild with Morphine Sulfate

Heart Failure Pneumonic

U Upright Position

N Nitrates

L Lasix

O Oxygen

A Amiodorone, ACE, ARBs

D Dig, Dobutamine

M Morphine Sulfate

E Extremities Up or Down

Definition

• CO=SVxHR is insufficient to meet the metabolic needs of the body

• SV is determined by preload, afterload and myocardial contractility

• Systolic failure- dec. contractility

• Diastolic failure- dec. filling

• EF< 40%

Heart Failure Etiology and Pathophysiology

• Systolic failure is the most common cause – Hallmark finding: Decrease in the left ventricular ejection

fraction (EF)• Caused by

– Impaired contractile function (e.g., MI)– Increased afterload (e.g., hypertension)– Cardiomyopathy– Mechanical abnormalities (e.g., valve disease)

http://coursewareobjects.elsevier.com/objects/mccance5e_v1/McCance/Module15/Part02/M15L04S41a.html??hostType=undefined&authorName=Mccance&prodType=undefined

Systolic Failure

hypokinesis

90/140= 64% EF- 55-65 normal

• Diastolic failure

– Impaired ability of the ventricles to relax and fill during diastole resulting in decreased stroke volume and CO

– Diagnosis based on the presence of pulmonary congestion, pulmonary hypertension, ventricular hypertrophy, normal ejection fraction (EF)

• Mixed systolic and diastolic failure– Seen in disease states such as dilated

cardiomyopathy (DCM)– Poor EFs (<35%)– High pulmonary pressures

• Biventricular failure (both ventricles may be dilated and have poor filling and emptying capacity)

Preload

• Volume of blood in ventricles at end diastole.

• Depends on venous return

• Depends on compliance

Afterload

• Force needed to eject the blood into the circulation

• Arterial B/P, pulmonary artery pressure

• Valvular disease increases afterload

• Pathophysiology

• A. Cardiac compensatory mechanisms– 1.tachycardia– 2.ventricular dilation-Starling’s law– 3.myocardial hypertrophy

• Hypoxia leads to dec. contractility

http://www.heartsite.CHF/html/chf_3.html

• B.Homeostatic compensatory mechanisms• Sympathetic Nervous System-(beta blockers block

this)– 1.vascular system- norepinephrine-

vasoconstriction(What effect on afterload?)– 2.kidneys-

• A. dec. CO and B/P cause renin angiotensin release.(ACE)• B. Aldosterone release causes Na and H2O retention• Inc. Na causes release of ADH(diuretics)• Release of atrial natriuretic factor- promotes Na and H20

excretion and prevents severe cardiac decompensation

– 3.liver- stores venous volume(ascites, +HJR,– Hepatamegaly- can store 10 L. check enzymes

• Compensatory mechanisms are activated to maintain adequate CO– Neurohormonal responses: Endothelin is

stimulated by ADH, catecholamines, and angiotensin II and causes• Arterial vasoconstriction• Increase in cardiac contractility• Hypertrophy

• Compensatory mechanisms are activated to maintain adequate CO– Neurohormonal responses: Proinflammatory cytokines

(e.g., tumor necrosis factor)

• Released by cardiac myocytes in response to cardiac injury

• Depress cardiac function by causing cardiac hypertrophy, contractile dysfunction, and myocyte cell death

• Compensatory mechanisms are activated to maintain adequate CO– Neurohormonal responses: Over time, a systemic

inflammatory response is mounted resulting in• Cardiac wasting• Muscle myopathy• Fatigue

• Counter regulatory processes

– Natriuretic peptides: atrial natriuretic peptide (ANP) and b-type natriuretic peptide (BNP)

• Released in response to increases in atrial volume and ventricular pressure

• Promote venous and arterial vasodilation, reducing preload and afterload

• Prolonged HF leads to a depletion of these factors

• Counter regulatory processes– Natriuretic peptides are endothelin and aldosterone

antagonists • Enhance diuresis • Block effects of the RAAS

– Natriuretic peptides inhibit the development of cardiac hypertrophy and may have antiinflammatory effects

Result of Compensatory Mechanisms

Heart Failure

PathophysiologyStructural Changes

• Decreased contractility

• Increased preload (volume)

• Increased afterload (resistance)

• Ventricular remodeling(ACE inhibitors can prevent this)– Ventricular hypertrophy– Ventricular dilation

Heart Failure- Hypertrophy

Ventricular remodeling

END RESULT

FLUID OVERLOAD AND EDEMA

Heart FailureClassification Systems

• New York Heart Association Functional Classification of HF– Classes I to IV

• ACC/AHA Stages of HF– Stages A to D

AHA Newer Classifications of Heart Failure- Staging

Stage A Those at high risk for developing heart failure. Includes people with:

•Hypertension •Diabetes mellitus •Coronary artery disease (including heart attack) •History of cardiotoxic drug therapy •History of alcohol abuse •History of rheumatic fever •Family history of CMP

•Exercise regularly •Quit smoking •Treat hypertension •Treat lipid disorders •Discourage alcohol or illicit drug use •If previous heart attack or current diabetes mellitus or hypertension angiotensin converting enzyme inhibitor (ACE-I)

Stage B Those diagnosed with “systolic” heart failure but have never had symptoms of heart failure (usually by finding an ejection fraction of less than 40% on echocardiogram).

•Care measures in Stage A + •All patients should be on ACE-I •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 current or prior symptoms. Symptoms include:

•Shortness of breath •Fatigue •Reduced exercise intolerance.

In this group, care measures from Stage A apply, ACE-I and beta-blockers should be used +

•Diuretics (water pills) •Digoxin •Dietary sodium (salt) restriction •Weight monitoring •Fluid restriction (as appropriate) •Withdrawal of drugs that worsen the condition •Spironolactone when symptoms remain severe with other therapies

Usual Therapies

Stage D Presence of advanced symptoms, after assuring optimized medical care

All therapies under Stages A, B and C + evaluation for:

•Cardiac transplantation •Ventricular assist devices •Surgical options •Research therapies •Continuous intravenous inotropic infusions •End-of-life care

• Primary risk factors– Coronary artery disease (CAD)– Advancing age

• Contributing risk factors – Hypertension– Diabetes– Tobacco use– Obesity– High serum cholesterol– African American descent– Valvular heart disease– Hypervolemia

Classifications

• Systolic versus diastolic– Systolic- loss of contractility get dec. CO– Diastolic- decreased filling or preload

• Left-sided versus right –sided– Left- lungs– Right-peripheral

• High output- hypermetabolic state• Acute versus chronic

– Acute- MI– Chronic-cardiomyopathy

Symptoms

Left Ventricular Failure

• Signs and symptoms– dyspnea

– orthopnea PND

– Cheyne Stokes

– fatigue

– Anxiety

– rales

– NOTE L FOR LEFT AND L FOR LUNGS

???????

• WHY DOES THIS OCCUR?

Heart FailureClinical Manifestations

• Acute decompensated heart failure (ADHF)– Pulmonary edema, often life-threatening

• Early – Increase in the respiratory rate – Decrease in PaO2

• Later – Tachypnea – Respiratory acidemia

• Acute decompensated heart failure (ADHF)• Physical findings

• Orthopnea• Dyspnea, tachypnea• Use of accessory muscles• Cyanosis• Cool and clammy skin

• Acute decompensated heart failure (ADHF)• Physical findings

• *Cough with frothy, blood-tinged sputum-why???

• Breath sounds: Crackles, wheezes, rhonchi • Tachycardia• Hypotension or hypertension

QuickTime™ and aYUV420 codec decompressor

are needed to see this picture.

Case study of Heart Failure in Lewis online resources

Pulmonary Edema(advanced L side HF)

• When PA WEDGE pressure is approx 30mmHg– Signs and symptoms

• 1.wheezing• 2.pallor, cyanosis• 3.Inc. HR and BP• 4.s3 gallop

The Auscultation Assistant - Rubs and Gallops

• 5.rales,copious pink, frothy sputum

Person literally drowning in secretions

Immediate Action Needed

Goals of Treatment

• MAD DOG

• Improve gas exchange– O2– intubate– elevate HOB– BIPAP

Right Heart Failure

• Signs and Symptoms

– fatigue, weakness, lethargy

– wt. gain, inc. abd. girth, anorexia,RUQ pain

– elevated neck veins

– Hepatomegaly +HJR

– may not see signs of LVF- why??

http://www.meddean.luc.edu/lumen/meded/MEDICINE/PULMONAR/IMAGES/movies/chan3.mov

Can Have RVF Without LVF

• What is this called and what causes it?

COR PULMONALE

This results from pulmonary hypertension.How does this affect

afterload?

Heart FailureComplications

• Pleural effusion

• Atrial fibrillation (most common dysrhythmia) – Loss of the atrial contraction (kick) can reduce

CO by 20% – Promotes thrombus/embolus formation

increasing risk for stroke– Treatment may include cardioversion,

antidysrhythmics, and/or anticoagulants

Heart FailureComplications

• High risk of fatal dysrhythmias (e.g., sudden cardiac death, ventricular tachycardia) with HF and an EF <35% (Use of ICDs and CRT)– HF can lead to severe hepatomegaly, especially

with RV failure • Fibrosis and cirrhosis can develop over time

– Renal insufficiency or failure

Heart FailureDiagnostic Studies

• Primary goal is to determine underlying cause– History and physical examination( dyspnea)– Chest x-ray– ECG– Lab studies (e.g., cardiac enzymes, BNP)

electrolytes– EF

Heart FailureDiagnostic Studies

• Primary goal is to determine underlying cause– Hemodynamic assessment-Hemodynamic

Monitoring-CVP- (right side) and SG(left and right side)

– Echocardiogram-TEE best– Stress testing- exercise or medicine– Cardiac catheterization- determine heart

pressures ( inc.PAW )– Ejection fraction (EF)

Transesophageal echocardiogram

Nursing Assessment

• Vital signs

• PA readings

• Urine output

• ----------------

• -----------------

• ----------------

Chronic HF Nursing Management

• Nursing diagnoses– Activity intolerance

– Decreased cardiac output

– Fluid volume excess

– Impaired gas exchange

– Anxiety

– Deficient knowledge

Decreased cardiac output

• Plan frequent rest periods• Monitor VS and O2 sat at rest and during activity• Take apical pulse• Review lab results and hemodynamic monitoring

results• Fluid restriction- keep accurate I and O• Elevate legs when sitting• Teach relaxation and ROM exercises

Activity Intolerance

• Provide O2 as needed

• practice deep breathing exercises

• teach energy saving techniques

• prevent interruptions at night

• monitor progression of activity

• offer 4-6 meals a day

Fluid Volume Excess

• Give diuretics and provide BSC

• Teach side effects of meds

• Teach fluid restriction

• Teach low sodium diet

• Monitor I and O and daily weights

• Position in semi or high fowlers

• Listen to BS frequently

Knowledge deficit

• Low Na diet

• Fluid restriction

• Daily weight

• When to call Dr.

• Medications

3 Main Goals- in acute as well as chronic HF

• Decrease preload

• Decrease afterload

• Increase contractility

How to Achieve Goals• Decrease preload

– Dec. intravascular volume-diuretics, natrecor

– Dec venous return• Fowlers

• MSO4 and Ntg

• Decrease afterload- – ACE (pril or ril),

– ARB (sartans),

– Vasodilators,

– beta blockers (al or ol)– BiDil (combination drug containing isosorbide dinitrate

and hydralazine) approved only for the treatment of HF in African Americans

Increase Contractility• Improve cardiac function

– For patients who do not respond to conventional pharmacotherapy (e.g., diuretics, vasodilators, morphine sulfate)

• Inotropic therapy – Digitalis -Adrenergic agonists (e.g., dopamine)– Phosphodiesterase inhibitors (e.g., milrinone) – Don’t give calcium channel blockers– New calcium sensitizer– CRT

• Balance supply and demand of oxygen– Inc. O2- O2, intubate, HOB up,Legs down,

mech vent with PEEP– Dec. demand-beta blockers, rest, dec B/P

Manage symptoms

Heart Failure Nursing and Collaborative Management • Overall goals of therapy for ADHF and

chronic HF

– Decrease patient symptoms

– Improve LV function

– Reverse ventricular remodeling

– Improve quality of life

– Decrease mortality and morbidity

PATIENT TEACHINGJoint Commission has mandated 6

areas of discharge teaching

Discharge Teaching6 areas

• Weight Monitoring

• Medications

• Activity

• Diet

• What to do if symptoms worsen

• Follow-up

Weight Monitoring

• Weight reduction recommendations must be individualized and culturally sensitive

• Same scale every day at same time

• Preferably in the morning after voiding

• Report weight gain of 3 or more pounds in two days or 3-5 or more in 1 week.

Activity

• Instruct patient in energy-conserving and energy-efficient behaviors

• Improves symptoms but often not prescribed • Cardiac Rehab program• Goal is 150 minutes per week• Walking, biking, swimming or a combo is

recommended

Diet• Nutritional therapy

– Diet and weight reduction recommendations must be individualized and culturally sensitive

– Dietary Approaches to Stop Hypertension (DASH) diet is recommended

• Avoid fats such as butter and margarine• Avoid fried foods• Read labels for hidden sodium

– Sodium is usually restricted to 2.5 g per day• Avoid any food with more than 400mg of sodium

– Alcohol- limit women 1 drink, men 2 drinks – Fluid restriction may or may not be not required

Medications– Medications (lifelong) diuretics, vasodilators, positive

inotropics

• Diuretics- loop, thiazides, spirinolactone (aldactone)

• Vasodilators- Ntg,

• Postive inotropics- digoxin

– Taking pulse rate

• Know when drugs (e.g., digitalis, -adrenergic

blockers) should be withheld and reported to health

care provider

• Home BP monitoring– Signs of hypo- and hyperkalemia if taking diuretics that

deplete or spare potassium

When to call Dr.

• Symptoms worsen– Shortness of breath– Edema– Weight gain– Side effects of medications– Chest pain

Follow-up

• Frequent follow-up with physician• Home health care may be needed

– Monitor symptoms– Effects of medications and side effects– Blood draws for potassium

• Other– Stop smoking– Flu and pneumonia vaccines– Refer to local support group

Chronic HF Collaborative Management

• Oxygen administration• Physical and emotional rest• Nonpharmacologic therapies

– Cardiac resynchronization therapy (CRT) or biventricular pacing

– Cardiac transplantation

CRT-Cardiac Resynchronization Therapy

HOW IT WORKS:

Standard implanted pacemakers are equipped with two wires (or "leads") that conduct pacing signals to specific regions of the heart (usually at positions A and C). The biventricular pacing devices have added a third lead (to position B) that is designed to conduct signals directly into the left ventricle. The combination of all three leads creates a synchronized pumping of the ventricles, increasing the efficiency of each beat and pumping more blood on the whole.

Chronic HF Collaborative Management

• Nonpharmacologic therapies (cont’d)– Intraaortic balloon pump (IABP) therapy – Ventricular assist devices (VADs)– Destination therapy—permanent, implantable

Surgical Interventions

• Intraaortic balloon pump (IABP)– Used for cardiogenic shock

– Allows heart to rest

• Ventricular assist device (VAD)– Takes over pumping for the ventricles

– Used as a bridge to transplant

Artificial Heart

Cardiomyoplasty-wrap latissimus dorsi around heart

Ventricular reduction surgery-ventricular wall is resected

Intraaortic Balloon Pump (IABP)

• Provides temporary circulatory assistance– ↓ Afterload– Augments aortic diastolic pressure

• Outcomes– Improved coronary blood flow– Improved perfusion of vital organs

Fig. 66-14

IABP Machine

Fig. 66-13

Enhanced External Counterpulsation-EECP

Pumps during diastole- increasing O2 supply to coronary arteries. Like IABP but not invasive.

The Cardiology Group, P.A.

Ventricular Assist Devices (VADs)

•• Indications for VAD therapyIndications for VAD therapy•• Extension of cardiopulmonary bypass Extension of cardiopulmonary bypass

•• Failure to weanFailure to wean

•• Postcardiotomy cardiogenic shock Postcardiotomy cardiogenic shock

•• Bridge to recovery or cardiac Bridge to recovery or cardiac transplantationtransplantation

Ventricular Assist Devices (VADs)

• Indications for VAD therapy (cont’d)– Patients with New York Heart Association

Classification IV who have failed medical therapy

Schematic Diagram of Left VAD

Fig. 66-16

New Heartmate

http://www.clevelandclinic.org/heartcenter/pub/guide/disease/heartfailure/lvad_devices.htm

Cardiomyoplasty technique: the left latissimus dorsi muscle(LDM) is transposed into the chest through a window created byresecting the anterior segment of the 2nd rib (5 cm). The LDM isthen wrapped arround both ventricles. Sensing and pacingelectrodes are connected to an implantable cardiomyostimulator

Cardiac Transplantation Nursing Management

• Treatment of choice for patients with refractory end-stage HF, inoperable CAD and cardiomyopathy

– Goal of the transplant evaluation process is to identify patients who would most benefit from a new heart

• Transplant candidates are placed on a list – Stable patients wait at home and receive

ongoing medical care – Unstable patients may require hospitalization

for more intensive therapy– The overall waiting period for a transplant is

long, and many patients die while waiting for a transplant

• Surgery involves removing the recipient’s heart, except for the posterior right and left atrial walls and their venous connections

• Recipient’s heart is replaced with the donor heart • Donor sinoatrial (SA) node is preserved so that a

sinus rhythm may be achieved postoperatively• Immunosuppressive therapy usually begins in the

operating room

• Infection is the primary complication followed by acute rejection in the first year after transplantation

• Beyond the first year, malignancy (especially lymphoma) and coronary artery vasculopathy are major causes of death

• Endomyocardial biopsies are obtained from the right ventricle weekly for the first month, monthly for the following 6 months, and yearly thereafter to detect rejection – Heartsbreath test is used along with endomyocardial

biopsy to assess organ rejection

• Peripheral blood T lymphocyte monitoring to assess the recipient’s immune status

• Care focuses on – Promoting patient adaptation to the transplant process– Monitoring cardiac function– Managing lifestyle changes– Providing relevant teaching

Blackboard Learning System™ (Release 6)

What’s New in Heart Failure?(myoblasts)

Heart Failure Center - Information on congestive heart failure symptoms and treatment information

Congestive Heart Failure: Overview

Heart failure case study

CHF case 4

http://www.austincc.edu/adnlev4/rnsg2331online/module04/heart_failure_case_study.htm

Practice Game

http://www.quia.com/cb/107511.html

Angiotensin-converting enzyme inhibitors , such as captopril and enalapril, block the conversion of angiotensin I to angiotensin II, a vasoconstrictor that can raise BP. These drugs alleviate heart failure symptoms by causing vasodilation and decreasing myocardial workload.

Beta-adrenergic blockers , such as bisoprolol, metoprolol, and carvedilol, reduce heart rate, peripheral vasoconstriction, and myocardial ischemia.

Diuretics prompt the kidneys to excrete sodium, chloride, and water, reducing fluid volume. Loop diuretics such as furosemide, bumetanide, and torsemide are the preferred first-line diuretics

because of their efficacy in patients with and without renal impairment. Low-dose spironolactone may be added to a patient's regimen if he has recent or recurrent symptoms at rest despite therapy with ACE inhibitors, beta-blockers, digoxin, and diuretics.

Digoxin increases the heart's ability to contract and improves heart failure symptoms and exercise tolerance in patients with mild to moderate heart failure.

Other drug options include nesiritide (Natrecor), a preparation of human BNP that mimics the action of endogenous BNP, causing diuresis and vasodilation, reducing BP, and improving cardiac output.

Intravenous (I.V.) positive inotropes such as dobutamine, dopamine, and milrinone, as well as vasodilators such as nitroglycerin or nitroprusside, are used for patients who continue to have heart failure symptoms despite oral medications. Although these drugs act in different ways, all are given to try to improve cardiac function and promote diuresis and clinical stability.

Prioritization and Delegation(22)

• Two weeks ago, a 63 year old client with heart failure received a new prescription for carvedilol (Coreg) 3.125 mg orally. Upon evaluation in the outpatient clinic these symptoms are found. Which is of most concern?

• A. Complaints of increased fatigue and dyspnea.

• B. Weight increase of 0.5kg in 2 weeks.

• C. Bibasilar crackles audible in the posterior chest.

• D. Sinus bradycardia, rate 50 as evidenced by the EKG.

• As the charge nurse in a long-term facility that has RN,LPN and nursing assistant staff members, a plan for ongoing assessment of all residents with a diagnosis of heart failure has been developed. Which activity is most appropriate to delegate to an LVN team leader?

• A. Weigh all residents with heart failure each morning• B. Listen to lung sounds and check for edema weekly.• C. Review all heart failure medications with residents

every month.• D. Update activity plans for residents with heart failure

every quarter.

• A cardiac surgery client is being ambulated when another staff member tells them that the client has developed a supraventricular tachycardia with a rate of 146 beats per minute. In what order will the nurse take these actions?

• A. Call the client’s physician.

• B. Have the client sit down.

• C. Check the client’s blood pressure.

• D. Administer oxygen by nasal cannula

• The echocardiagram indicates a large thrombus in the left atrium of a client admitted with heart failure. During the night, the client complains of severe, sudden onset left foot pain. It is noted that no pulse is palpable in the left foot and that it is cold and pale. Which action should be taken next?

• A. Lower his left foot below heart level.

• B. Administer oxygen at 4L per nasal cannula.

• C. Notify the physician about the assessment data.

• D. Check the vital signs and pulse oximeter.

• The nurse is caring for a hospitalized client with heart failure who is receiving captopril (Capoten) and spironolactone (aldactone). Which lab value will be most important to monitor?

• A. Sodium• B. Blood urea nitrogen (BUN)• C. Potassium• D. Alkaline phosphatase (ALP)

heart failure by nancy jenkins the most common reason for hospitalization in adults >65 years...

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