心力衰竭教学幻灯片讲义.ppt

Treatment of Heart Failure Angiotensin Converting-Enzyme Inhibitors (ACEI): Survival SAVE (Survival and Ventricular Enlargement). Mortality curves in the SAVE study in patients with varying degrees of post-infarct ventricular dysfunction. In this study, 2231 patients with EF 40% were randomized to receive captopril or placebo between 3 to 16 days after experiencing a transmural infarct. After 42 months, the captopril group had a significant reduction in overall mortality (-19%), number of reinfarctions (-25%), hospitalizations (-22%), and in the number of patients who developed clinical congestive heart failure. The mortality reduction appeared after 1 year of treatment. Pfeffer MA et al. Survival and Ventricular Enlargement (SAVE) Study. NEngl J Med 1992;327:669. Treatment of heart failure. Digoxin: Pharmacokinetics Oral absorption is 60-75% of the administered dose; when given by this route, maximal levels are reached after 30-90 minutes and its action is maximal after 3-6 h. When given i.v., onset of action is at 5-30 min and this reaches its maximum at 2-4 h. It is approximately 25% bound to plasma proteins and is widely distributed through the body, crossing the blood brain barrier and the placenta. It accumulates in skeletal muscle, liver and heart, where it may reach concentrations that are 10 to 50 times higher than serum levels. This explains why hemodialysis eliminates little of the digoxin load in digoxin toxicity. Cardiac uptake of digoxin increases in patients with hypokalemia and decreases in the presence of hyperkalemia, hypercalcemia or hypomagnesemia. Digoxin undergoes very little biotransformation, and is mainly eliminated through glomerular filtration and somewhat by tubular secretion. In patients with renal insufficiency, the half life of digoxin increases 2-4 times, so that the maintenance dose must be determined according to the creatinine clearance, generally requiring half of the usual dose and, in severe cases, intermittent dosi