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Digitalis medicines strengthen the force of the heartbeat by increasing the amount of calcium in the heart’s cells. (Calcium stimulates the heartbeat.) When the medicine reaches the heart muscle, it binds to sodium and potassium receptors.
The main mechanism of action of digitalis is on the sodium-potassium ATPase of the myocyte. It reversibly inhibits the ATPase resulting in increased intracellular sodium levels. The build-up of intracellular sodium leads to a shift of sodium extracellularly through another channel in exchange for calcium ions.
Cardiac glycosides are a class of organic compounds that increase the output force of the heart and increase its rate of contractions by acting on the cellular sodium-potassium ATPase pump. They are selective steroidal glycosides and are important drugs for the treatment of heart failure and cardiac rhythm disorders.
Digitalis produces an increase of blood flow, a decrease of vascular resistance, venodilation, and a decrease of central venous pressure and heart rate (Figure 1). The vasodilation is the result of an increase in cardiac output and direct baroreflex-mediated withdrawal of sympathetic vasoconstriction.
By increasing the concentration of intracellular calcium or increasing the sensitivity of receptor proteins to calcium, positive inotropic agents can increase myocardial contractility.
Specific inhibition of the Na+ pump by digitalis induces a positive inotropic effect by increasing the intracellular Na+ concentration which in turn induces an increase in the intracellular Ca2+ concentration by the Na+/Ca2+ exchange and an increase in the Ca2+ pool of the sarcoplasmic reticulum; toxic effects are …
The end-point of digoxin’s effect is to open membrane calcium channels, resulting in an increased calcium influx into cells. When the calcium levels are high, in the setting of digoxin toxicity, the result is an increase in calcium influx and enhanced toxicity.
Digitalis is a cholinergic agonist, a chemical compound with properties like acetylcholine or the parasympathetic nervous system.
| Table 1: Baseline Treatments at Randomization in the PARADIGM-HF Drug Trial♦ | ||
|---|---|---|
| Medication | Control Group | Treatment Group |
| Digoxin | 31.2% | 29.2% |
Digitalis compounds are potent inhibitors of cellular Na+/K+-ATPase. This ion transport system moves sodium ions out of the cell and brings potassium ions into the cell.
Cardiac glycosides are a class of medications that inhibit the Na+ K+ ATPase enzyme, increasing the force of heart contractions. The most commonly prescribed cardiac glycoside is digoxin, which can be used to treat atrial fibrillation, atrial flutter, and congestive heart failure.
Conclusions: Digoxin significantly decreases diastolic blood pressure during overnight sleep in patients with congestive heart failure. This effect is likely to be caused by reduction of sympathetic activity or increase of parasympathetic activity.
Digoxin, also called digitalis, helps an injured or weakened heart pump more efficiently. It strengthens the force of the heart muscle’s contractions, helps restore a normal, steady heart rhythm, and improves blood circulation. Digoxin is one of several medications used to treat the symptoms of heart failure.
After intravenous administration, amiodarone acts to relax smooth muscles that line vascular walls, decreases peripheral vascular resistance (afterload), and increases the cardiac index by a small amount. Administration by this route also decreases cardiac conduction, preventing and treating arrhythmias.
Increasing contractility is done primarily through increasing the influx of calcium or maintaining higher calcium levels in the cytosol of cardiac myocytes during an action potential.
Pharmacologic agents: Drugs which increase cardiac contractility are called positive inotropic agents. Examples of these are dopamine, adrenalin and digoxin.
Briefly, an increase in venous return to the heart increases the filled volume (EDV) of the ventricle, which stretches the muscle fibers thereby increasing their preload. This leads to an increase in the force of ventricular contraction and enables the heart to eject the additional blood that was returned to it.
Emesis is one of the most common symptoms of poisoning with the members of the digitalis group. All of the digitalis bodies are capable of causing emesis, but the different members of the group apparently show much greater differences in emetic, than in cardiac, activity with a given species of animal.
Digitalis also exerts three primary effects on Purkinje fibres – it decreases resting potential resulting in slowed phase 0 depolarization and thus conduction, It decreases action potential duration which increases sensitivity to electrical stimulation; and it enhances automaticity due to increased rate of phase 4 …
The main route of elimination is renal excretion of digoxin, which is closely correlated with the glomerular filtration rate. In addition, some tubular secretion and perhaps tubular reabsorption occurs. Nearly all of the digoxin in the urine is excreted unchanged, with a small part as active metabolites.
Digoxin increases the force of contraction of the muscle of the heart by inhibiting the activity of an enzyme (ATPase) that controls movement of calcium, sodium, and potassium into heart muscle. Calcium controls the force of contraction.
A low level of potassium in the body can increase the risk of digitalis toxicity. Digitalis toxicity may also develop in people who take digoxin and have a low level of magnesium in their body.
2. Digoxin in increasing doses slowed the heart rate at rest; with the daily dose of 0.50 mg from 63 +/- 10 to 53 +/- 6 beats min-1, and fractional shortening rose from 28 +/- 6 to 33 +/- 3% (P less than 0.05 for both). Preload, afterload and cardiac output did not change.
We show that PDE inhibition by atropine promotes an increase in intracellular cAMP, which in turn leads to an elevated heart rate and increased contractility. This effect of atropine is clearly independent of M1/2/3-muscarinic receptors and does not involve its classical anticholinergic activity.
Digoxin was one of the first identified RORγT receptor inverse agonists inhibiting the differentiation of Th17 cells. However, this compound exhibits inhibitory activity at relatively high concentrations that mediate cytotoxic effects.
The parasympathetic limb of the autonomic nervous system is most sensitive to these effects of digitalis, and its properties are significantly altered with therapeutic concentrations of the drug. These actions are particularly important in mediating the electrophysiologic effects of digitalis.
It is concluded that oral digoxin improves left ventricular ejection fraction in elderly patients with congestive heart failure or cardiomegaly who are in sinus rhythm. Some of these patients achieve maximal improvement in ejection fraction at serum digoxin concentrations of less than 1.0 ng/ml.
Digitalis decreased circulating plasma volume. Yes. Decreased circulating plasma volume in only part of the explanation. Increased ejection fraction also contributes to the decrease in venous pressure because decreased ventricular chamber volume and diastolic pressure result in decreased venous filling pressure.
Furthermore, digitalis has a positive inotropic and antiarrhythmogenic effect. Specific binding sites for digitalis glycosides have been observed in erythrocytes, the myocardium and the central nervous system.
Dobutamine is a synthetic catecholamine that acts on alpha-1, beta-1 and beta-2 adrenergic receptors. In the heart, the stimulation of these receptors produces a relatively strong, additive inotropic effect and a relatively weak chronotropic effect.
Not only the myocardial digoxin kinetic is changed during hypokalemia but the renal excretion rate of digoxin is markedly reduced during hypokalemia leading to increased serum digoxin concentration and thereby the risk of digitalis intoxication.
Cardiac glycosides suppress enhanced atrioventricular conduction and do not affect it provided it remains within normal. The mechanisms by which cardiac glycosides may act are discussed: extracardiac, cholinomimetic (in the acute test and direct one) and influencing heart conduction components (when used continuously).
Digitoxin is a cardiac glycoside used in the treatment and management of congestive cardiac insufficiency, arrhythmias and heart failure.
Vasodilator and inotropic drugs work through independent mechanisms in augmenting left ventricular pump function in patients with heart failure. The selection between these two classes of pharmacologic agents for an individual patient may be based on the control blood pressure as well as the underlying disease.
Chemicals taken from foxglove are used to make a prescription drug called digoxin. Digitalis lanata is the major source of digoxin in the US. Foxglove is most commonly used for heart failure and fluid build up in the body (congestive heart failure or CHF) and irregular heartbeat (atrial fibrillation).
Digoxin is a type of drug called a cardiac glycoside. Their function is to slow your heart rate down and improve the filling of your ventricles (two of the chambers of the heart) with blood. For people with atrial fibrillation, where the heart beats irregularly, a different volume of blood is pumped out each time.
Hyperkalemia is the usual electrolyte abnormality precipitated by digoxin toxicity, primarily in the acute setting. Hyperkalemia may be associated with acute renal failure that subsequently precipitates digoxin toxicity.