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INTRODUCTION
Congestive heart failure, according to Mayo Clinic occurs when the heart muscle doesn't pump
blood as well as it should. When this happens, blood often backs up and fluid can build up in the lungs,
causing shortness of breath. Furthermore, Certain heart conditions, such as narrowed arteries in the heart
(coronary artery disease) or high blood pressure, gradually leave the heart too weak or stiff to fill and
pump blood properly. Heart failure often develops after other conditions have damaged or weakened the
heart. However, heart failure can also occur if the heart becomes too stiff.
Signs and Symptoms
Signs and symptoms of congestive heart failure may include breathlessness during activity (most
commonly), at rest, or while sleeping, which may come on suddenly and wake you up, fatigue and
weakness, swelling in the legs, ankles and feet, rapid or irregular heartbeat , reduced ability to exercise
persistent cough or wheezing with white or pink blood-tinged mucus, swelling of the belly area
(abdomen), very rapid weight gain from fluid buildup, nausea and lack of appetite, difficulty
concentrating or decreased alertness, chest pain if heart failure is caused by a heart attack.
Causes
Heart failure can start suddenly after a medical condition or injury damages your heart muscle.
But in most cases, heart failure develops slowly from long-term medical conditions.
Conditions that can cause heart failure include:
Right-sided heart failure Fluid may back up into the abdomen, legs and
feet, causing swelling.
Systolic heart failure (also called heart failure The left ventricle can't contract vigorously,
with reduced ejection fraction) indicating a pumping problem.
Heart failure with preserved ejection fraction The left ventricle can't relax or fill fully,
indicating a filling problem.
PATHOPHYSIOLOGY
Congestive heart failure is a syndrome that can be caused by a variety of abnormalities, including
pressure and volume overload, loss of muscle, primary muscle disease or excessive peripheral demands
such as high output failure. In the usual form of heart failure, the heart muscle has reduced contractility.
This produces a reduction in cardiac output, which then becomes inadequate to meet the peripheral
demands of the body. The 4 primary determinants of left ventricular (LV) performance are generally
altered as follows: (1) There is an intrinsic decrease in muscle contractility. (2) Preload or left atrial filling
pressure is increased, resulting in pulmonary congestion and dyspnea. (3) Although systemic blood
pressure is often reduced, there is an increase in systemic vascular resistance (afterload), which can
further reduce cardiac output. (4) Heart rate is generally increased as part of a compensatory mechanism
associated with an increase in sympathetic tone and circulating catecholamines. In patients with coronary
disease, there is often an imbalance between myocardial oxygen supply and demand. An increase in heart
size may be particularly deleterious by increasing wall tension because of the Laplace relation and
increasing myocardial oxygen consumption.
TREATMENT OPTIONS
Heart failure is a chronic disease needing lifelong management. However, with treatment, signs and
symptoms of heart failure can improve, and the heart sometimes becomes stronger.
Doctors sometimes can correct heart failure by treating the underlying cause. For example, repairing a
heart valve or controlling a fast heart rhythm may reverse heart failure. But for most people, treatment of
heart failure involves a balance of the right medications and, sometimes, use of devices that help the heart
beat and contract properly.
MEDICAL INTERVENTION
Medical Intervention
Indication Nursing
Drug Classification Action Dosage
responsibilities
Furosemide Loop diuretics PO: ELDERLY: Inhibits reabsorption 20mg Check vital
(Lasix) Initially, 20–80 of sodium, and PO signs, esp. B/P,
mg/dose; may chloride in ascending daily pulse, for
increase by 20–40 loop of Henle and hypotension
mg/ dose q6–8h. proximal/distal renal before
May titrate up to tubules. administration.
600 mg/ day in Assess
severe edematous Therapeutic Effect: baseline renal
states. Increases excretion function, and
of water, sodium, serum
chloride, electrolytes,
magnesium, and esp. serum
calcium. sodium, and
potassium.
Initiate I & O
monitoring
Digoxin Cardiac PO: ELDERLY: Inhibits 0.125 Assess apical pulse
(Lanoxin) glycoside 0.125–0.25 mg sodium/potassium mg PO before
once daily. ATPase pump in daily administration.
myocardial cells. Monitor ECG for
Promotes calcium arrhythmias for 1–
influx. Therapeutic 2 hours after
Effect: Increases administration
contractility. (excessive slowing
of the pulse may be
the first clinical
sign of toxicity).
Assess for GI
disturbances, and
neurologic
abnormalities
(signs of toxicity).
Monitor serum
potassium,
magnesium,
calcium, and renal
function.