HEART FAILURE

• Affects nearly 5 million Americans

• Estimated 400,000-700,000 diagnosed annually since 1979
• Less than 50% alive after 5 years, less than 25% after 10 years
• Heart Failure (HF) is the most common admitting dx for hospital admissions over age 65

Risk Factors:
1. CAD (ischemic)
2. HTN
3. DM
4. Obesity
5. Smoking
6. Hyperlipidemia
7. Obstructive sleep apnea

Perfusion: supplying an organ or tissue with nutrients and oxygen via the blood through the arteries

HEART FAILURE is a syndrome that results from pump failure, heart unable to pump adequate amounts of blood
to meet the body’s metabolic needs

Systolic versus Diastolic:

Systolic: ventricles not contracting with enough force (pump) blood out to the rest of the body during systole
(emptying)
o Ejection Fraction <40%
o Wall thickness decreased
o S&S: Decreased exercise tolerance, dyspnea, congestion, and/or pulmonary edema

Diastolic: ventricles not able to relax or fill properly, less enters heart, contracts normally
o Ejection Fraction > 50%
o Wall thickness: increased
o S&S: Decreased exercise tolerance, dyspnea, congestion, and/or pulmonary edema

Principles of Blood Flow

o CARDIAC OUTPUT
o CO = SV x HR
o CO (cardiac output) is the amount of blood ejected by the left ventricle into the aorta in one minute,
approx 5.25 L/min
o SV (stroke volume) amount of blood ejected during each ventricular contraction, 70-75 ml
o HR (heart rate) number of times the heart beats per min

Ejection Fraction
o The percentage of blood remaining in the ventricle after diastole (relaxation)
o Normal 50-70%
o Diastolic Failure: EF > 50%
o Systolic Failure: EF < 40%

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 PRELOAD
o Volume of blood that fills the heart with each beat
o Larger the PRELOAD, the greater the stroke volume

AFTERLOAD
o The resistance the heart has to pump against to eject blood from the heart
o Also know as systemic vascular resistance (SVR)

CONTRACTILITY
o The ability of the heart muscle to contract and eject blood from the heart
o Inotropic: positive or negative

FRANK STARLING LAW

o Cardiac performance which states that the force of contraction of the cardiac muscle is proportional to its
initial length. (The energy set free at each contraction is a simple function of cardiac filling (preload).
o When the diastolic filling of the heart is increased or decreased with a given volume, the displacement of
the heart increases or decreases with this volume.)

PATHOPHYSIOLOGY OF HEART FAILURE:

Increased Preload
o Too much volume
o Impaired contractility of the muscle causing inability of the heart muscle to eject the blood. The LVEDV
will be increased

Decreased Contractility
o Muscle too weak to contract
o Muscle is hypertrophied or stretched out and not able to effectively contract

Increased Afterload
o Increased resistance the heart has to pump against. This will lead to an increase in LVEDP

CAUSES OF HEART FAILURE

• ISCHEMIC
o Coronary Artery Disease
o Myocardial infarction
• DIALATED / NON-ISCHEMIC
o Hypertension
o Valvular Disorder
o Alcohol/Drug Abuse
o Viral
o Pregnancy
o Adriamycin Toxicity

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HEART FAILURE: LEFT VERSUS RIGHT:
Left Sided HF
o Most common
o Left ventricular dysfunction (MI, HTN, cardiomyopathy)
o Back up of blood into the left atrium and pulmonary system
o Signs and symptoms:
 SOB
 Pulmonary congestion
 Orthopnea/PND
 Decreased Cardiac Output
 Edema
Right-sided HF
o Left-sided HF, right ventricular MI, cor pulmonale-R ventricular hypertrophy and failure r/t pulmonary
HTN
o Back up of blood into right atrium and venous systemic circulation
o Signs and symptoms:
 Jugular venous distention (JVD)
 Hepatomegaly
 Splenomegaly
 Ascites
 Peripheral edema

COMPENSATORY MECHANISMS
• Frank-Starling Mechanism
o The greater the stretch the greater the force of contraction
o Increases contractile force
o Limited by overstretching, increases myocardial O2 demand
• Neurohormonal
o SNS
 Catecholemine release (epi, norepi)
 Increased HR, BP, contractility, vascular resistance (peripheral vasoconstriction), venous return
 Tachycardia decreases filling time, CO; increased vascular resistance, myocardial work and O2
demand
o RAAS (Renin-Angiotensin-Aldosterone System
 Stimulated by decreased CO and decreased renal perfusion
 Kidneys release Renin
 Angiotensinogen to angiotensin I to angiotensin II: increases peripheral vasoconstriction
 Angiotensin II causes Adrenal cortex release Aldosterone: sodium and water retention
 Increased preload and afterload, pulmonary congestion, fluid retention
o Endothelin
 stimulated by ADH, catecholemines, and angiotensin II
 Arterial vasoconstriction, cardiac contractility, hypertrophy
 Hypertrophy, ventricular wall thickening
o ADH (Antidiuretic Hormone )
 Released from posterior pituitary
 Water excretion inhibited, increased blood volume
 Fluid retention, increased preload and afterload, pulmonary congestion
• Natriuretic Peptides (ANP,BNP)
o Increased vascular volume and pressure in the atrial and ventricles releases ANP, BPN
o Promote sodium and water excretion (diuresis)
o Blocks effects of RAAS
o Too weak to counteract the vasoconstriction and water retention in HF
• Ventricular Hypertrophy
o Cardiac muscle cells enlarge, wall thickens
o Poor contractility, higher O2 needs, poor coronary circulation, prone to ventricular dysrhythmias
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 • Ventricular remodeling
o Dilation in response to stretch and pressure
• Activated to maintain CO
• Compensate to a point
• Detrimental over time as they increase myocardial oxygen demand and workload

DIAGNOSTICS:
• Echocardiogram
o Wall motion, thickens, valvular fx, LV fx
o Ejection Fraction:
o N= >50%, HF =,40%
• Cardiopulmonary Exercise Testing
• Stress testing
• BNP: N<100
• Cardiac Catheterization
• Biopsy of myocardium
• Hemodynamic measurement: pressures and volumes, CO, SVR

COMPLICATIONS:
• Dysrhythmias
o Ventricular: non-sustained VT, lethal dysrhythmias resulting in death
o Atrial Fibrillation: loss of atrial kick, decrease CO 20-30%
• Renal Insufficiency
o Poor CO leads to decreased blood flow to kidneys
o Leads to failure
• Worsening DM

NY Heart Association Functional Class

• NYHA I: No symptoms with any activity
• NYHA II: Symptoms with exertion
• NYHA III: Symptoms with minimal activity
• NYHA IV: Symptoms at rest
STAGES:
• Stage A: Risk factors for HF such as HTN, DM, CAD, Family Hx, Obesity
• Stage B: Structural heart disease but no symptoms of HF
• Stage C: Structural heart disease with prior or current symptoms
• Stage D: Refractory or end-stage. Requiring specialized intervention
ACUTE DECOMPENSATED HEART FAILURE
CLINICAL MANIFESTATIONS:
1. Orthopnea
2. Dyspnea
3. Tachypnea
4. Use of accessory muscles
5. Cyanosis
6. Cool, clammy skin
7. Cough
8. Frothy, blood tinged sputum
9. Tachycardia
10. Hypotension or hypertension
11. Pulmonary edema: increased RR rate, decreased 02 sat, resp acidosis

CHRONIC DECOMPENSATED HEART FAILURE

CLINICAL MANIFESTATIONS:
1. Fatigue
2. Dysnpea
3. Orthopnea
4. PND

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 5. Persistent, dry cough
6. Weight gain: .2-3 lb in 2 days or 5lbs in 7 days
7. Dependent edema
8. Nocturia
9. Cool, dusky, damp skin
10. Restless, confused, decreased memory
11. Chest pain
12. Anorexia, nausea

COLLABORATIVE MANAGEMENT
GOALS:
• Reverse remodeling
• Down regulate neurohormonal activation
• Decrease patient symptoms
• Improve LV function
• Improve quality of life
• Decrease mortality and morbidity

TREATMENT OPTIONS:
• Medical therapy
• BiV pacing
o Decrease wall stress
• Temporary assist device
o Tandom Heart
o Cancion Device(clinical trial)
• Surgical Therapy
• VADs
o Pneumatic
o Axial Flow
• Transplant

MECHANICAL ASSIST DEVICE:

• Right and Left Ventricular Devices
• Indications
o Post-cardiotomy recovery/Bridge to Recovery
o Bridge to transplant
o Destination therapy

DRUG THERAPY:

ACE INHIBITORS
• All pts with current or prior symptoms
• Captopril, enalapril, fosinopril, quinapril, lisnopril
• Monitor renal fx
o Lower dose with renal insufficiency in Stage C/D
o Renal protective
o Monitor for hyperkalemia
ARBS
• Used in pt who are ACE intolerant or due to cough
• Block angiotensin II at receptor site
• Valsartan, candesartan, hyzaar, cozaar

BETA BLOCKERS
• Decrease HR, BP, force of contraction, slows impulses,
• Suppresses secretion of renin
• Bisprolol, carvedilol, metoprolol

DIURETICS
• Maintain euvolemic status
• Loop diuretics
• Furosemide, torsemide, bumex
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 • Can develop resistance
• Monitor daily weight, dietary restrictions, dose adjustments, BUN/CR

INOTROPICS
• Increase force of contraction, slow rate
• Digoxin
• Monitor volume status, toxicity
• Narrow therapeutic range
• Monitor potassium, hypokalemia can lead to toxicity
• Apical pulse

ALDOSTERONE ANTAGONIST
• Block effects of aldosterone
• Potassium sparing
• Monitor renal fx, potassium level
• Aldactone/spironolactone, eplerenone/inspra

VASODILATORS
• Cause vasodilation, lowers BP, and pulmonary pressure w/ R-sided HF
• Nitrates, hydralazine
• Combination hydralazine and isosorbide dinitrate (Bidil) for African Americans

NURSING COLLABORATIVE
MANAGEMENT:
• Improve cardiac function
o For patients who do not respond to conventional pharmacotherapy (e.g., diuretics, vasodilators, morphine
sulfate)
o Inotropic therapy
 Digitalis
 β-Adrenergic agonists (e.g., dopamine)
 Phosphodiesterase inhibitors (e.g., milrinone)
• Hemodynamic monitoring
• Decrease venous return (preload)
o Reduces the amount of volume returned to the LV during diastole
 High-Fowler’s position
 IV nitroglycerin
• Decrease intravascular volume
o Reduces venous return and preload
 Loop diuretics (e.g., furosemide)
 Ultrafiltration or Dialysis
• Improve gas exchange and oxygenation
o Supplemental oxygen
o Morphine sulfate
o Noninvasive ventilatory support (BiPAP)
• Decrease afterload
o Improves CO and decreases pulmonary congestion
o IV sodium nitroprusside (Nipride)
o Morphine sulfate
o Nesiritide (Natrecor)

NURSING ASSESSMENT
• Subjective data
o Past Health History
o Functional Health Patterns
o Current Medications
• Objective data
o RESPIRATORY
 Rate, rhythm, labored, number of pillows used, orthopnea, PND
 Lung Sounds: crackles, “wet”

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 o SKIN
 Warm vs cool
 Dry vs clammy
o PERIPHERAL VASCULAR
 Pulses: radial, pedal
 Capillary refill: brisk, sluggish
o NEUROLOGICAL
 LOC, orientation
o FLUID VOLUME STATUS
 JVD, hepatomegaly, N/V/D, Urine Output, peripheral edema

NURSING DIAGNOSIS:
1. Altered tissue perfusion
2. Activity intolerance
3. Fluid volume excess
4. Impaired gas exchange
5. Anxiety
6. Deficient knowledge

PATIENT EDUCATION:
• Medication
o Take as prescribed
o Actions and SE
o Taking pulse rate and when medications (digoxin, beta blockers) should be held
• Sodium Restriction
o 2000 mg
o 2 teaspoons per day
o DASH Diet
• Fluid restriction
o 64 ounces per day
o Measure in 2 liter bottle
• Daily weights
o Same time, same clothes, same scale
o 2-3 lbs/day OR
o 5 lbs in one week
o Can be first sign of exacerbation
• Activity
o Plan to minimize fatigue, rest periods
• DVT prophylaxis
o Compression stockings
o Mobilize fluid, decrease dependent edema
• Signs of ACUTE exacerbation
o Increase fatigue, SOB
o Weight gain
o Abdominal distention, change in appetite
o Chest discomfort
• Quality of LIFE
• Palliative Care
• Living Will
• Hospice