congestive heart failure(redirected from Congestive heart failure-etiology)
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Characteristics of the failure to thrive syndrome include lack of physical growth (for example, weight and height below the third percentile for age) and below normal achievement in fine and gross motor, social-adaptive, and language skills as assessed by psychometric testing using a tool such as the Denver Developmental Screening Test. Additionally, the child with this syndrome displays withdrawing behavior, avoidance of eye contact, and stiffness or flaccid posture when held. These children often have a history of irritability, feeding problems, and disturbed sleep patterns.
Parents of infants with failure to thrive syndrome typically display feelings of concern and inadequacy. The infant who is feeding poorly and is irritable may elicit a response in the caregiver that reflects tension and frustration. The need for comfort and nurturing by the infant may not be met, and this may lead to a cycle that exacerbates feeding problems.
Intervention encompasses identification of infants and mothers at risk for the syndrome and care of both mother or primary caregiver and infant. The major goals are to encourage the mother to express her feelings without fear of rejection, to model the role of mother and teach her nurturing behaviors, and to promote her self-esteem and confidence. Important nursing goals in the care of the infant include providing optimal nutrition, comfort, and rest; meeting the infant's psychosocial needs; and supplying emotional nurturance and sensory stimulation appropriate to the assessed developmental level.
There are three general kinds of pathologic conditions that can bring about congestive heart failure: (1) ventricular failure, in which the contractions of the ventricles become weak and ineffective, as in myocardial ischemia from coronary artery disease; (2) mechanical failure of the ventricles to fill with blood during the diastole phase of the cardiac cycle, which can occur when the mitral valve is narrowed, as in rheumatic mitral stenosis, or when there is an accumulation of fluid within the pericardial sac (cardiac tamponade) pressing against the ventricles, preventing them from accepting a full load of blood; and (3) an overload of blood in the ventricles during the systole phase of the cycle. High blood pressure, aortic stenosis, and aortic regurgitation are some of the conditions that can cause ventricular overload.
First, the failing heart attempts to maintain a normal output of blood by enlarging its pumping chambers so that they are capable of holding a greater volume of blood. This increases the amount of blood ejected from the heart, but it also leads to fluid overload within the blood vessels and excessive accumulation of body fluids in all of the fluid compartments.
Second, the heart begins to increase its muscle mass in order to strengthen the force of its contractions. This results in ventricular hypertrophy and a need for more oxygen. Eventually, the coronary arteries can no longer meet the oxygen demands of the enlarged myocardium and the patient experiences angina pectoris owing to ischemia.
Third, there is a response from the sympathetic nervous system. The involuntary muscle of the heart is regulated by autonomic, or involuntary, innervation. In response to failing contractility of the myocardial cells, the sympathetic nervous system activates adaptive processes that increase the heart rate, redistribute peripheral blood flow, and retain urine. These mechanisms are responsible for the symptoms of diaphoresis, cool skin, tachycardia, cardiac arrhythmias, and oliguria.
The combined efforts of these three compensatory mechanisms achieve a fairly normal level of cardiac output for a period of time. During this phase of congestive heart failure, the patient is said to have compensated CHF. When these mechanisms are no longer effective the disease progresses to the final stage of impaired heart function and the patient has decompensated CHF.
Fluid retention is another common symptom of congestive heart failure. In left-sided failure there is higher than normal pressure of blood in the pulmonary vessels. This increased pressure forces fluid out of the intravascular compartment and into the tissue spaces of the lungs, causing pulmonary edema. Right-sided failure causes congestion in the capillaries of the peripheral circulation and results in edema and congestion of the liver, stomach, legs, and feet, and in the sacral region in bedridden patients.
Decreased cardiac output also affects the kidneys by reducing their blood supply, which in turn causes a decrease in the rate of glomerular filtration of plasma from the renal blood vessels into the renal tubules. Sodium and water not excreted in the urine are retained in the vascular system, adding to the blood volume. The diminished blood supply to the kidney also causes it to secrete renin, which indirectly stimulates the secretion of aldosterone from the adrenal gland. Aldosterone in turn acts on the renal tubules, causing them to increase reabsorption of sodium and water, and thus to further increase the volume of body fluids.
See also: forward heart failure, backward heart failure, right ventricular failure, left ventricular failure. Synonym(s): cardiac failure, cardiac insufficiency, congestive heart failure, myocardial insufficiency
congestive heart failure
congestive heart failureCongestive heart disease Cardiology '…a complex clinical syndrome characterized by abnormalities of left ventricular function and neurohormonal regulation, which are accompanied by effort intolerance, fluid retention, and reduced longevity'; an impairment of cardiac function in which failing ventricles cannot adequately perfuse tissue to meet metabolic demands; CHF usually develops over a long period, but may be abrupt in onset Epidemiology CHF is a major health problem which affects 2-3 million, US; 400,000 new cases are diagnosed/yr Clinical Low-output 'forward CHF'–weakness, fatigue, lethargy, light-headedness, and confusion; in decompensated CHF, cardiac cachexia ensues, characterized by exhaustion and loss of lean muscle mass; low-output backward CHF–pulmonary congestion–fluids accumulate in lungs, causing dyspnea, initially only on exertion; also seen, peripheral and pedal edema, rales, S3 gallop, sinus tachycardia, hypotension, ↑ jugular venous pressure, and abdominojugular–hepatojugular reflux High-output heart failure–'non-cardiac' CHF Albright's disease–polyostotic fibrous dysplasia, anemia, carcinoid syndrome, arteriovenous fistulas–trauma, Paget's disease of bone, hemangiomatosis, glomerulonephritis, hemodialysis, liver disease–alcohol-related thiamin deficiency, ↓ peripheral arterial resistance, hyperkinetic heart syndrome, polycythemia vera, thyrotoxicosis CHF precipitants Alcohol, cor pulmonale, drug-related–inappropriate medications, non-compliance, ↑ fluid and/or sodium intake, fever, hypothyroidism, hypoxia, infection, obesity, pregnancy, pulmonary embolism, renal failure, uncontrolled HTN Workup-EKG–to exclude myocardial ischemia or infarction, and/or arrhythmia Workup-lab CBC–to exclude anemia, BUN and creatinine–to assess renal function, electrolytes–K+ and magnesium, liver enzymes, cardiac markers including enzymes–eg, LDH isoenzymes and proteins–e.g., troponin T–to exclude recent MI or ischemia, thyroid function tests–to exclude thyrotoxicosis, a major cause of high-output heart failure Radiology Cardiac enlargement, interstitial and/or alveolar edema, and pulmonary vascular redistribution in acute CHF, findings which are less common in chronic CHF Echocardiography–M-mode, 2-D, & Doppler to determine the left ventricular ejection fraction; CHF typically has concentric left ventricular hypertrophy Management of precipitating factors Eliminate noncardiac factors–eg, alcohol, drugs, excess fluid and/or sodium intake, fever, hypothyroidism, hypoxia, infection, renal insufficiency, HTN, and other factors; control precipitating factors, which may eliminate the signs and symptoms of CHF Acute management Acute CHF with extreme respiratory distress is a medical emergency that requires immediate treatment to ↓ volume–preload and myocardial O2 demand and ↑ forward blood flow Long-term management Once CHF develops, it requires continuous therapy to ↓ M&M–ie,
heart fail·ure(hahrt fāl'yŭr)
See also: forward heart failure, backward heart failure, right ventricular failure, left ventricular failure
Synonym(s): cardiac insufficiency, congestive heart failure, myocardial insufficiency.
congestive heart failureSee HEART FAILURE.
Congestive heart failure
heart fail·ure(hahrt fāl'yŭr)
Patient discussion about congestive heart failure
Q. What Is the Treatment for Congestive Heart Failure? My mother is 76 years ols and has been suffering from a heart disease for many years. Lately she has developed congestive heart failure. How is this situation treated?
"Congestive heart failure has been strongly correlated with significantly low blood and tissue levels of CoQ10 ....
[In numerous studies] treatment with CoQ10 significantly improved heart muscle function while producing no adverse effects or drug interactions."
Q. congestive heart failure how it works is it to do with fluid built up in your body
As blood flow out of the heart slows, blood returning to the heart through the veins backs up, causing congestion in the tissues. Often swelling (edema) results. Most often there's swelling in the legs and ankles, but it can happen in other parts of the body, too. Sometimes fluid collects in the lungs and interferes with breathing, causing shortness of breath, especially when a person is lying down.
Heart failure also affects the kidneys' ability to dispose of sodium and water. The retained water increases the edema.
Q. describe the symptoms of congestive heart failure