Añorve GA, Sánchez RE

Language: Spanish
References: 14
Page: 31-38
PDF size: 143.45 Kb.

ABSTRACT

In normal conditions, the heart has seven kinds of receptors on the cellular membrane surface which in normal conditions can be activated by several chemical and hormonal stimuli as for instance parcelary ischemic necrosis, due to myocardial failure, hemodynamic excessive over load without structural harm as in the case of aortic insufficiency whatever the cause, heart failure reduces expulsion fraction increases the ventricular volumenes and lowers cardiac “waste”. The decrease of the expulsion fraction becomes the trigger mechanism to liberate (generate) the compensatory mechanisms (“catecolamins” and “reninas” secretion). It has been demonstrated that if the cause of heart failure is not remedied the neurohumoral system remains persistently activated and it is the cause of the illness progression. The present pharmacological treatment for heart failure is meant to avoid the perpetuation of these neurohumoral mechanisms and, thus, avoid the progression of this illness and improve morbi-mortality of patients who suffer from it.
The most important knowledge that sustains the present heart failure therapy is summaryzed is this work so that the nurse can satisfy the demands of nowadays clinical world and come-up with short, and long-term strategies which aim at the efficient attainment of established goals for the patient.

REFERENCES

1. Massie BM, Shah NB. Evolving trends in the epidemiology of heart failure a rationale for prevention. Am Heart J. San Francisco, California. 1997; 133: 703-12.

2. Kalon H, Anderson K, Kannel WB, Grossman W, Levy D. Survival after the onset of congestive heart failure in Framingham heart study subjects. Boston. Circulation 1993; 88: 107-15.

3. Benedict CCR, Weiner DDH, Johnstone DDE et al. Comparative neurohormonal responses in patients with preserved and impaired left ventricula ejection fraction: result of the studies of left ventricular dysfunction (SOLVD Registry). Carolina del Norte, J Am Coll Cardiol 1993; 22(Suppl. A): 146A-153A.

4. Francis GS, Go1dsmith SSR, Olivari BMT et al. The neurohumoral axis in congestive heart failure. Minesotta. Ann Intern Med 1984; 101: 370-7.

5. Mason DT. Regulation of cardiac peformance on clinical heart disease congestive heart failure, mechanisms, evaluation and treatment. York Med Book, 1976.

6. Paolisso G. Metabolic and cardiovascular benefits driving from beta adrenergic blockade in chronic congestive heart failure. Nápoles. Am Hearth J 1992; 123: 103-110.

7. Ribner HS, Zucker MJ, Stacior C et al. Vasodilators as first-line therapy for congestive heart failure: A comparative hemodynamic of hydralazine, digoxine and their combination. Chicago, Illinois. Am Heart J 1987; 114: 91-6.

8. MD Ader R, Chatterjee Kanu, MB Ports Thomas et al. Immediate and sustained hemodynamic and clinical improvement in chronic heart failure by an oral angiotensin-converting enzyme inhibitor. San Francisco, California. Circulation 1980; 61: 93-7.

9. Young JB, Uretzky BF, Shandihi E et al. On behalf of the PROVED study investigators multicenter double blind placebo-controlled randomized. Withdrawal case of the efficacy end safely of digoxin in patients with mild and moderate chronic heart failure not treated with converting enzymes inhibitor (Abstract). Dallas, Texas, J Am Coll Cardiol 1992; 19(Suppl.): 259-A.

10. Waagstein F, Hjalmorson A, Ivarmauskas A et al. Effect of chronic beta-adrenergic receptor blockade in congestive cardiomyopathy. Sweden. Brit Heart J 1975; 37: 1022-36.

11. Bristow MR, Ginsburg R, Umans V et al. B1-B2-Adrenergic- receptor subpopulations in nonfailing and failing human ventricular myocardium: coupling of both receptor subtypes to muscle constriction and selective Beta 1-receptor down-regulation in heart failure. Stanford, California. Circ Res 1986; 59: 297-309.

12. Bristow MR, Gingsburg R, Minobe W et al. Decrease catecholamine, sensibility and Beta-adrenergic receptor density in failing human heart. Stanford, California. N Engl J Med 1982; 307: 205-211.

13. Packer M, Colucci WS, Sackner-Berstein Jonathan D et al. Precise study group. Double blind, placebo-controlled study of the effects of carvedilol in patients with moderate to severe heart failure. New York. The Precise trial, Circulation 1996; 94: 2793-2799.

14. Israili ZH, Hall D. Cough and angioneurotic edema associated with angiotensin-converting enzyme inhibitor therapy: a review of literature and pathopysiology. Atlanta, Georgia. Ann Inter Med 1992; 117: 234-42.