Managing Chronic Heart Failure

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Transcript Managing Chronic Heart Failure

Managing Chronic
Heart Failure
By Janet Riggs RN, CCRN, CCNS, MSN
Nursing made Incredibly Easy! January/February 2006
2.5 ANCC/AACN contact hours
Online: www.nursingcenter.com
© 2006 by Lippincott Williams & Wilkins. All world rights reserved.
Defining Heart Failure

Heart unable to supply enough oxygen-carrying blood to
meet the metabolic needs of the body

Begins with an injury to the myocardium that affects the
ventricles’ ability to fill/eject blood

Remodeling occurs; process of dilation/hypertrophy of
one or both of the ventricles
Types of Heart Failure

Low-output heart failure-Left ventricle unable to eject
enough blood, due to weakness caused by MI,
pulmonary hypertension

High-output heart failure-Volume of blood exceeds
what ventricle can eject, resulting in back-up of blood
and dilation of ventricle; causes: mitral valve
regurgitation, aortic valve insufficiency, hyperthyroidism,
anemia, hypervolemia
Types, continued

Biventricular failure-Back-up pressure from failing left
ventricle causes dilation/failure of right ventricle

Left ventricular systolic dysfunction-Heart muscle too
weak to contract fully

Left ventricular diastolic dysfunction-Left ventricle
becomes stiff and can’t fill adequately
Causes

Coronary artery disease & hypertension responsible for
2/3 of heart failure cases

Remaining cases caused by non-ischemic
cardiomyopathy related to:
• thyroid dysfunction
• valvular heart disease
• cardiotoxic substances: alcohol, cocaine,
chemotherapy
• idiopathic or unknown
Heart Failure Stages: ACC/AHA



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Stage A: Patients are at risk for heart failure, but have
no symptoms or structural changes; typically have
diabetes, hypertension, coronary artery disease.
Stage B: Patients have a documented structural heart
change but no symptoms yet; may have hx of MI, valve
regurgitation, left ventricular hypertrophy.
Stage C: Patients with structural changes and
symptoms.
Stage D: Patients with refractory heart failure; may
require mechanical or pharmaceutical support, a
transplant, or end-of-life care.
NYHA Classification System


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Class 1: Ordinary physical activity doesn’t cause undue fatigue,
dyspnea, or anginal pain.
Class II: Asymptomatic at rest, slight limitations of physical activity.
Ordinary physical activity causes palpitations, dyspnea, & anginal
pain.
Class III: Marked limitations of physical activity, but asymptomatic at
rest. Less-than-ordinary physical activity causes fatigue,
palpitations, dyspnea, or anginal pain.
Class IV: Patient unable to perform physical activity without
discomfort, may have symptoms at rest. This patient will be
considered for mechanical or pharmaceutical support, heart
transplant or end-of-life care.
Components of Cardiac Output

Stroke volume consists of:
• preload
• afterload
• contractility
Compensatory Mechanisms

Cardiac output=stroke volume x heart rate
One of the body’s mechanisms to compensate is to
release norepinephrine & epinephrine to increase HR,
which increases cardiac output.
Another mechanism is the renin-angiotensinaldosterone system, which senses decreased blood
volume to the kidneys and activates a series of events to
increase fluid volume and blood pressure.
More Compensation

Another mechanism is to increase stroke volume by
increasing the amount of fluid in the bloodstream.

Release of two amino acids: human atrial natriuretic
peptide (hANP) & human brain natruiretic peptide
(hBNP); both released by “stretch” receptors in the
atria and ventricles, respectively, in response to
increased blood volume; purpose: to lose excess fluid
volume, which decreases BP and improves blood flow
through the coronary arteries.
Signs & Symptoms

Left-sided heart failure
• Lung “crackles”
• Tachycardia
• Low SpO2
• Paroxysmal nocturnal
dyspnea
• GI symptoms: nausea,
bloating, constipation
• Cool/cold/pale/cyanotic
extremities
• Weight gain

Right-sided heart failure
• Jugular venous
distention
• Liver engorgement
• Ascites
• Peripheral edema
• Weight gain
Diagnostics


Transthoracic echocardiogram (TEE): Most common &
effective diagnostic tool
Coupled with Doppler flow studies, TEE can show
atrial/ventricular hypertrophy, valve problems, where
problem is located (inside or outside the heart), and
when problem occurs (systole or diastole)

12-lead ECG, chest X-ray, MRI, CT scan

R & L heart catheterization
Treatment

Decrease preload
• Diuretics
• Aldosterone
antagonists
• ACE inhibitors
• Natrecor

Decrease afterload
• Vasodilators
• ACE inhibitors
Treatment, continued

Decrease
myocardial
workload

Decrease ventricular
remodeling
• Beta-blockers
• ACE inhibitors
• Beta-blockers

Optimize
contractility
• Digoxin
Treatment, continued:

Afterload-Deflation after blood leaves;
determined by ventricular pressure, blood
volume, & wall thickening

Contractility-Contraction of the myocardium to
force blood out of the heart
Nursing Interventions

Monitor vital signs/daily weights

Instruct patient about their medical therapy

Instruct patient regarding sodium restriction

Instruct patient regarding positions of comfort (semiFowler’s)
More Nursing Interventions

Stress importance of contacting HCP about weight gain
of 2 lbs or more/day or 5 lbs in a week or if awakened
with dyspnea

If patient smokes, provide smoking cessation info

Teach caution using NSAIDs due to sodium retention,
myocardial depression