Congestive Heart Failure
Congestive Heart Failure or CHF is a condition where there is weakening in the pumping action of the heart due to fluid buildup in the body. The term 'congestive' is indicative of the blood backing up into the liver, abdomen, lungs or lower extremities. This medical condition develops over a period of time and leads to enlargement of the heart. Due to the inability to pump enough blood, the heart compensates by becoming larger. This leads to enlarged heart chambers and thicker heart wall muscles. Persons suffering from coronary disease or arrhythmia are more at risk for CHF.
Persons suffering from hypertension and heart valve disease are more susceptible to congestive heart failure. If you have suffered a heart attack or congenital heart defect, you are more likely to be prone to CHF. Congestive heart failure is characterized by backing up of the blood from both one or both the lower chambers of the heart.
Symptoms of Congestive heart failure include shortness of breath and weakness. A person suffering from CHF may notice weight gain on account of body fluid accumulation. This shows up as water retention and edema in the ankles, feet and legs. The fluid buildup leads to frequent urination, especially at night. Chest pain, irregular pulse and restlessness are other symptoms of CHF. Decreased alertness and inability to pursue exercise are signs of congestive heart failure. There is weakness and extreme fatigue due to reduced blood flow to the major organs. Dizziness and confusion is noticed due to inadequate oxygen supply to the brain. Persistent cough and wheezing can also be noticed.
Diagnostic tests such as chest x-rays and ECG can aid in detecting any stress on the heart. During a physical examination, a doctor can detect fluid buildup in the chest. Imaging tests such as angiography and nuclear ventriculorgraphy help in clear diagnosis of the heart's pumping condition. EKG and echocardiogram aids in detecting any possible heart enlargement and fluid buildup. Blood tests can indicate any kidney or thyroid malfunction that may affect heart's functioning. BNP test or B-type natriuetic peptide Test is conducted to assess heart failure.
Medications for congestive heart failure include ACE inhibitors that keep the blood vessels open and inotropics to strengthen the heart's pumping capacity. Diuretics may be prescribed to get rid of excess body fluids. Vasodilators and Calcium channel blockers open up narrowed blood vessels. Angioplasty is done to open up narrowed arteries. This is resorted to in cases where there is fatty plaque buildup. Surgery to repair existing defects such as heart valve repair and coronary artery surgery are sometimes resorted to. Lifestyle changes can go a long way in keeping CHF at bay. CHF is a progressive condition; it cannot be cured but lifestyle changes can go a long way in slowing the progress of the disease. These include quitting smoking and controlling diabetes, cholesterol and high blood pressure. Control alcohol consumption and embark on a fitness regimen that includes aerobic exercise.
Acardia is a rare and serious malformation that occurs exclusively in monizygous twins - twins developing from a single egg. Acardia represents one of the most severe and rare congenital anomalies. It is characterized by the absence of functioning heart. Acardia results from the artery to artery connections in the placenta, thereby causing a physically normal fetus to circulate blood for itself as well as a severely malformed fetus suffering from heart regression. In other words, fetus acardius is a parasite and it receives blood supply from the donor twin. Because the pump twin heart has to pump for two, there is a high risk of going into heart failure and this would lead to the death of the normal twin.
The most common variety is the acardius acephalus where the head is lacking and so are the upper extremities. Other types are acardius anceps, acardius acormus and acardius amorphous. While in acardius anceps, the most highly developed form, a partly developed head with remnants of cranial bones and brain tissue are present with developed body and extremities, acardius acormus is the rarest form of acardia. The monster is a head without a body. Acardia amorphous is the least developed monster not recognizable as a human form, with minimally developed visceral organs. Since there is no gross human form, the name acardius amorphous.
As to the cause of acardia, the etiology of acardiac monster is still unknown. Genetic defects have been reported to be the cause. Some researchers suggest chromosomal abnormalities to be the reason. Krause and Bejdl suggest that compression of the cephalic pole of the embryo prohibiting curving and fusion of the primitive heart tube to be the basic cause of this anomaly. As a result, the dependant entodermal organs like thyroid, esophagus, trachea, lung, liver and others are also not formed.
A pregnant woman carrying an acardiac twin is unlikely to have any unusual symptoms. An acardiac twin is often found incidentally on prenatal ultrasound. As no two acardiac twins are formed exactly alike, they may present differently. Several improved imaging techniques like 2D ultrasonography, 3D ultrasonography and transvaginal Doppler ultrasonography have made diagnosis of acardia possible even in the first trimester of pregnancy. Such early diagnosis helps to reduce the risk of complications. Fetal echocardiography is also recommended to assist in early detection of heart failure in the normal twin. Chromosome studies are also done on both fetuses.
One line of treatment is watching for the earliest signs of heart failure in the pump twin with frequent ultrasounds. If heart failure is identified and the pregnancy is also far enough, then the pump twin should simply be delivered. Physicians recommend prenatal interruption of the blood vessel connections before heart failure develops in the pump twin, thus sacrificing the acardiac twin.
Specialists use laser, electrical cauterization and electrodes, serial amniocentesis, medications and other treatments successfully. If the acardiac twin is large enough and the amount of blood flow to it can cause heart failure in the healthy twin, then blood flow is stopped with Fetal Image-Guided Surgery. The acardiac or parasitic twin never survives, as it is severely malformed and does not have a functioning heart. The normal twin is at risk for heart failure and complications associated with premature birth. The normal twin is expected to have about 10% risk for malformations.
BNP blood test
The brain natriuretic peptide or BNP blood test measures the level of B-Natriuretic Peptide in your blood. This protein hormone is produced in excess when the heart's ventricles are not functioning properly. When there is heart failure, the ventricles secrete BNP and N-terminal-pro-BNP (NT-pro-BNP). Natriuretic peptides promote better blood circulation, urine excretion and heart functioning. Both BNP and NT—Pro BNP are markers of atrial and ventricular distension caused due to raised intra-cardiac pressure.
Typically, the BNP test helps determine if a person is suffering heart failure, when there are symptoms that can be indicative of other conditions too. Blood BNP levels are also indicative of the exercise tolerance and risk of death in a person suffering from CHF (congestive heart failure).
You may need to fast for about 10 hours prior to a BNP blood test. BNP blood test is usually measured by the Triage test and the test usually takes about 15 minutes. The elevated BNP values indicate the severity of the heart condition. While BNP levels below 100 pg/mL indicate no heart failure, BNP levels above 600 pg/mL indicate moderate heart failure. The diagnostic gray area of levels between I00 and 500 pg/mL shows inconclusive result. If BNP levels are above 900 pg/mL, it is indicative of severe heart failure. Medication affects the levels of BNP. BNP values tend to be elevated with increasing age and noticed to be higher in women than men. Conditions such as chronic obstructive pulmonary disease (COPD), kidney disease or kidney dialysis can alter the BNP blood readings.
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Collection of Pages - Last revised Date: December 6, 2023