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Heart failure cardiac glycosides

Patients with congestive heart failure must have increased cardiac output while decreasing the workload on the damaged heart. The cardiac glycosides are most frequently used to enhance cardiac output. This class of drugs appears to work by increasing the... [Pg.325]

ACE inhibitors can be administered with diuretics (qv), cardiac glycosides, -adrenoceptor blockers, and calcium channel blockers. Clinical trials indicate they are generally free from serious side effects. The effectiveness of enalapril, another ACE inhibitor, in preventing patient mortaUty in severe (Class IV) heart failure was investigated. In combination with conventional dmgs such as vasodilators and diuretics, a 40% reduction in mortaUty was observed after six months of treatment using 2.5—40 mg/d of enalapril (141). However, patients complain of cough, and occasionally rash and taste disturbances can occur. [Pg.129]

The outcome of this is to couple ATP hydrolysis with the vectorial transport of Na+ and K+ across the plasma membrane. The inhibition of the (Na+-K+)-ATPase by cardiac glycosides such as digitalis (an extract of foxglove leaves), which blocks the dephosphorylation of the E2-P form of the enzyme, is the basis for a number of steroid drags which are commonly prescribed for the treatment of congestive heart failure. [Pg.158]

Secondary hypotension is a sign of an underlying disease that should be treated first. If stroke volume is too low, as in heart failure, a cardiac glycoside can be given to increase myocardial contractility and stroke volume. When stroke volume is decreased due to insufficient blood volume, plasma substitutes will be helpful in treating blood loss, whereas aldosterone deficiency requires administration of a mineralocor-ticoid (e.g., fludrocortisone). The latter is the drug of choice for orthostatic hypotension due to autonomic failure. A parasympatholytic (or electrical pacemaker) can restore cardiac rate in bradycardia. [Pg.314]

Cardiac glycosides are drags used in the treatment of congestive heart failure or cardiac arrhythmia, by inhibiting the Na+/K+ pump. This inhibition increases the amount of Ca + ions available for contraction and improves cardiac output and reduces distention of the heart. Cardiac glycosides are extracted from plant material. [Pg.237]

In summary, cardiac glycosides increase contractile force and reduce heart rate and AV conduction. In addition, cardiac glycosides suppress the sympathetic hyperactivity which occurs in advanced stages of congestive heart failure via a complex mechanism involving the central nervous system. [Pg.339]

Myocardial cell membrane ATPase, the enzyme present in heart muscle, is the site of action of the cardiac steroid glycosides, which have a specific action on the heart muscle. These drugs increase the force of contraction of the muscle (positive inotropic effect) as well as its conductivity and automaticity. They are also valuable in treating congestive heart failure, in which the circulatory needs of organs are no longer satisfied, and heart arrhythmias, in which the rhythm of the cardiac contractions is upset. The effect of the drug is that the force of contraction increases and the heart rate is slowed (chronotropic effect). Consequently, the cardiac output is elevated while the size of the heart decreases. [Pg.492]

The net result of the action of therapeutic concentrations of a cardiac glycoside is a distinctive increase in cardiac contractility (Figure 13-5, bottom trace). In isolated myocardial preparations, the rate of development of tension and of relaxation are both increased, with little or no change in time to peak tension. This effect occurs in both normal and failing myocardium, but in the intact patient the responses are modified by cardiovascular reflexes and the pathophysiology of heart failure. [Pg.307]

In patients with left ventricular dysfunction but no edema, an ACE inhibitor should be used first. Several large studies have showed clearly that ACE inhibitors are superior to both placebo and to vasodilators and must be considered, along with diuretics, as first-line therapy for chronic heart failure. However, ACE inhibitors cannot replace digoxin in patients already receiving the drug because patients withdrawn from the cardiac glycoside deteriorate while on ACE inhibitor therapy. [Pg.312]

Digoxin is indicated in patients with heart failure and atrial fibrillation. It is also most helpful in patients with a dilated heart and third heart sound. It is usually given only when diuretics and ACE inhibitors have failed to control symptoms. Only about 50% of patients with normal sinus rhythm (usually those with documented systolic dysfunction) will have relief of heart failure from digitalis. Better results are obtained in patients with atrial fibrillation. If the decision is made to use a cardiac glycoside, digoxin is the one chosen in most cases (and the only one available in the USA). When symptoms are mild, slow loading (digitalization) with 0.125-0.25 mg per day is safer and just as effective as the rapid method (0.5-0.75 mg every 8 hours for three doses, followed by 0.125-0.25 mg per day). [Pg.312]

N.A. Convallaria majalis L. C. sepium L. Cardiac glycosides, cardenolides, convallotoxin, convalloside, convallatoxol, flavonoid glycosides." Affect in heart failure, regulate heart beat, lower blood pressure. [Pg.260]

Crude leaf preparations of Digitalis have been in medical use since 1785. Pure cardiac glycosides are now available. These preparations in injectable tinctures or powdered leaf tablets are used extensively for the treatment of congestive heart failure. They increase the force of the heart muscle and the power of systolic contraction, apparently by inhibiting the active transport of K and Na ions through cell membranes. [Pg.735]

The key experiment was one which would not be carried out until Skou learned of a paper published in German four years earlier, which showed that the movement of cations across the red cell membrane was inhibited by cardiac glycosides such as ouabain, plant alkaloids used for some 200 years in the therapy of heart failure. In 1957, Skou was unaware of this important finding, and wrote later that he had not done the crucial experiment to show Na/K ATPase as the transport system. When done, the experiment was decisive ouabain inhibited the ATPase activity exactly as it did the cation fluxes. This led to a flurry of activity in many biochemical laboratories and allowed Skou (nine years after his original publication) to write a review in which he concluded that the enzyme fulfilled the requirements for a system responsible for active transport of Na+ and K+ across the cell membrane. Thus the Na/K ATPase had the following properties ... [Pg.259]


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See also in sourсe #XX -- [ Pg.120 , Pg.121 , Pg.122 , Pg.122 , Pg.123 , Pg.123 , Pg.124 , Pg.125 ]




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