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 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 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-angiotensin-aldosterone 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 • Tachycardia • Low SpO2 • 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 Decrease afterload • Vasodilators • Diuretics • Aldosterone antagonists • ACE inhibitors • Natrecor Decrease afterload • Vasodilators • ACE inhibitors

Treatment, continued Decrease myocardial workload • Beta-blockers Decrease ventricular remodeling • Beta-blockers • ACE inhibitors 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 (semi-Fowler’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