Drug Treatment Heart Failure
Drug Treatment Heart Failure
Heart Failure – Definition, Causes, Symptoms and Treatment
Heart failure also called is congestive heart failure. Heart failure becomes more common with advancing age. Heart failure is a condition in which the heart can’t pump enough blood throughout the body. Heart failure is a condition in which the heart can’t pump enough blood throughout the body. Heart failure develops over time as the pumping action of the heart grows weaker. Heart failure is a serious condition. It contributes to or causes about 300,000 deaths each year. About 5 million people in the U.S. have heart failure. It contributes to 300,000 deaths each year. It can affect the left side, the right side, or both sides of the heart. Most cases involve the left side where the heart can’t pump enough oxygen-rich blood to the rest of the body. The most common causes of heart failure are hypertension (high blood pressure) and coronary artery disease (for example, you have had a heart attack). Arterial plaque lines the inside of the arteries that supply the heart and the rest of the body, meaning less blood gets to the heart itself, as well as the heart having to work harder to push blood through the thinner systemic arteries.
Heart failure may result from disorders that cause the heart’s walls to stiffen, such as infiltrations and infections. Heart failure due to systolic dysfunction usually develops because the heart cannot contract normally. Heart failure has two main forms: systolic dysfunction (which is more common) and diastolic dysfunction. In systolic dysfunction, the heart contracts less forcefully and cannot pump out as much of the blood that is returned to it as it normally does. Heart valve disorders—narrowing (stenosis) of a valve, which hinders blood flow through the heart, or leakage of blood backward (regurgitation) through a valve—can cause heart failure. Some heart valve disorders, such as aortic valve stenosis, hinder blood flow out of the heart. Other causes may include diseases of the heart valves and weakened heart muscle due to viral infections or their poisonous products (called toxins). Individuals with heart failure are sensitive to small shifts in their intravascular volume status (the amount of fluid in their circulatory system). Often left heart failure leads to right heart failure and then both sides are affected.
Left-sided heart failure leads to fluid accumulation in the lungs, which causes shortness of breath. Heart failure is a major cause of sudden death due to production of arrhythmias. Persons with diabetes have a much greater risk of developing heart failure than those without because diabetes is associated with other heart failure risk factors such as high blood pressure, obesity and high cholesterol levels. Weight reduction – through physical activity and dietary modification, as obesity is a risk factor for heart failure and ventricular hypertrophy. Fluid restriction – patients with CHF have a diminished ability to excrete free water load. Sodium restriction – excessive sodium intake may precipitate or exacerbate heart failure. Moderate physical activity, when symptoms are mild or moderate; or bed rest when symptoms are severe. Another current treatment involves the use of left ventricular assist devices (LVADs). Smoking and drinking alcohol can worsen heart failure and should be stopped. Exercise, weight loss, and stopping smoking help reduce the risk of coronary artery disease, as do good control of diabetes and lowering of cholesterol levels.
Treatment for Heart Failure Tips
1. Angiotensin-converting enzyme (ACE) inhibitors drugs help people with heart failure live longer and feel better.
2. Diuretics are often called “water pills” because they make you urinate more often and help keep fluid from building up in your body.
3. Diuretics, or water tablets, which work on the kidneys to remove the extra fluid and salt from the body and lower blood pressure.
4. ACE (angiotensin converting enzyme) inhibitors, which lower blood pressure and help the heart to pump more easily.
5. Digoxin helps the heart by making it beat more strongly and pump more blood.
6. Nitrates help with shortness of breath because they reduce the blood pressure in the lungs by widening (dilating) blood vessels and allow the heart to work more efficiently.
7.Warfarin stops blood clots from forming and Aspirin also stops blood clots from forming
About the Author
Juliet Cohen writes articles for online medical clinic and diseases treatment. She also writes articles on stress treatment.
what is the status of digoxin now in treatment of heart failure?
is digoxin the drug number one in human usage of drugs?
The main pharmacological effects of digoxin are on the heart. Extracardiac effects are responsible for many of the adverse effects which are below
Its main cardiac effects are
* A decrease of conduction of electrical impulses through the AV node, making it a commonly used drug in controlling the heart rate during atrial fibrillation or atrial flutter.
* An increase of force of contraction via inhibition of the Na+/K+ ATPase pump
Mechanism of action Digoxin binds to a site on the extracellular aspect of the α-subunit of the Na+/K+ ATPase pump in the membranes of heart cells (myocytes). This causes an increase in the level of sodium ions in the myocytes, which then leads to a rise in the level of calcium ions. The proposed mechanism is the following: inhibition of the Na+/K+ pump leads to increased Na+ levels, which in turn slows down the extrusion of Ca2+ via the Na+/Ca2+ exchange pump. Increased amounts of Ca2+ are then stored in the sarcoplasmic reticulum and released by each action potential, which is unchanged by digoxin. This is a different mechanism from that of catecholamines. Digoxin also increases vagal activity via its central action on the central nervous system, thus decreasing the conduction of electrical impulses through the AV node. This is important for its clinical use in different arrhythmias. Today, the most common indications for digoxin are probably atrial fibrillation and atrial flutter with rapid ventricular response. High ventricular rate leads to insufficient diastolic filling time. By slowing down the conduction in the AV node and increasing its refractory period, digoxin can reduce the ventricular rate. The arrhythmia itself is not affected, but the pumping function of the heart improves owing to improved filling. The use of digoxin in congestive heart failure during sinus rhythm is controversial. In theory the increased force of contraction should lead to improved pumping function of the heart, but its effect on prognosis is disputable and digoxin is no longer the first choice for congestive heart failure. However, it can still be useful in patients who remain symptomatic despite proper diuretic and ACE inhibitor treatment. Digoxin is usually given by mouth, but can also be given by IV injection in urgent situations (the IV injection should be slow, heart rhythm should be monitored). The half life is about 36 hours, digoxin is given once daily, usually in 125 μg or 250 μg dosing. In patients with decreased kidney function the half life is considerably longer, calling for a reduction in dosing or a switch to a different glycoside (such as digitoxin which although having a much longer elimination half-life of around 7 days, is mainly eliminated from the body via the liver, and thus not affected by changes in renal function). Effective plasma levels are fairly well defined, 1-2.6 nmol/l. In suspected toxicity or ineffectiveness, digoxin levels should be monitored. Plasma potassium levels also need to be closely controlled. The occurrence of adverse drug reactions is common, owing to its narrow therapeutic index (the margin between effectiveness and toxicity). Adverse effects are concentration-dependent, and are rare when plasma digoxin concentration is <0.8 μg/L. They are also more common in patients with low potassium levels (hypokalemia), since digoxin normally competes with K+ ions for the same binding site on the Na+/K+ ATPase pump. Common adverse effects (≥1% of patients) include: loss of appetite, nausea, vomiting, diarrhoea, blurred vision, visual disturbances (yellow-green halos), confusion, drowsiness, dizziness, nightmares, agitation, and/or depression. Less frequent adverse effects (0.1%–1%) include: acute psychosis, delirium, amnesia, shortened QRS complex, atrial or ventricular extrasystoles, paroxysmal atrial tachycardia with AV block, ventricular tachycardia or fibrillation, heart block but when sytematically sought, the evidence for this is equivocal. The pharmacological actions of digoxin usually results in electrocardiogram (ECG) changes, including ST depression or T wave inversion, which do not indicate toxicity. PR interval prolongation, however, may be a sign of digoxin toxicity. Additionally, increased intracellular Ca2+ may cause a type of arrhythmia called bigeminy (coupled beats), eventually ventricular tachycardia or fibrillation. The combination of increased (atrial) arrhythmogenesis and inhibited atrio-ventricular conduction (for example paroxysmal atrial tachycardia with A-V block - so-called "PAT with block") is said to be pathognomonic (i.e. diagnostic) of digoxin toxicity. An often described but rarely seen adverse effect of digoxin is a disturbance of colour vision (mostly yellow and green colour) called xanthopsia. Digoxin has an interaction with the antimalarial medication Hydroxychloroquine. Other informationDigoxin has potentially dangerous interaction with verapamil, amiodarone and erythromycin. In overdose, the usual supportive measures are needed. If arrhythmias prove troublesome, or malignant hyperkalaemia occurs (inexorably rising potassium level due to paralysis of the cell membrane bound ATPase-dependant Na/K pumps), the specific antidote is antidigoxin (antibody fragments against digoxin, trade name Digibind®). Digoxin is not usefully removed by hemodialysis.Some physical properties of digoxin are water solubility of 64.8 mg/L at 25 °C and melting point at 249.3 °C.
DEATH BY ADDICTION (HEART FAILURE BY SIXX AM)
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