Managing Chronic Heart Failure

download report

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
© 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
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,
• idiopathic or unknown
Heart Failure Stages: ACC/AHA
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
Stage D: Patients with refractory heart failure; may
require mechanical or pharmaceutical support, a
transplant, or end-of-life care.
NYHA Classification System
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
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
• GI symptoms: nausea,
bloating, constipation
• Cool/cold/pale/cyanotic
• Weight gain
Right-sided heart failure
• Jugular venous
• Liver engorgement
• Ascites
• Peripheral edema
• Weight gain
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
Decrease preload
• Diuretics
• Aldosterone
• ACE inhibitors
• Natrecor
Decrease afterload
• Vasodilators
• ACE inhibitors
Treatment, continued
Decrease ventricular
• Beta-blockers
• ACE inhibitors
• Beta-blockers
• 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