A perspective on diuretic resistance in chronic congestive heart failure

Chronic congestive heart failure (CHF) is a complex disorder characterized by inability of the heart to keep up the demands on it, followed by the progressive pump failure and fluid accumulation. Although the loop diuretics are widely used in heart failure (HF) patients, both pharmacodynamic and pharmacokinetic alterations are thought to be responsible for diuretic resistance in these patients. Strategies to overcome diuretic resistance include sodium intake restriction, changes in diuretic dose and route of administration and sequential nephron diuretic therapy. In this review, we discuss the definition, prevalence, mechanism of development and management strategies of diuretic resistance in HF patients.

Download Full-text

Mechanism and management of diuretic resistance in congestive heart failure

Journal of Dhaka National Medical College & Hospital ◽

10.3329/jdnmch.v17i1.12193 ◽

2012 ◽

Vol 17 (1) ◽

pp. 44-46

Author(s):

Dipankar Chandra Nag ◽

AKM Murshed ◽

Rajashis Chakrabortty ◽

Md Raziur Rahman

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Sodium Intake ◽

Diuretic Therapy ◽

Compensatory Hypertrophy ◽

Loop Diuretics ◽

Thick Ascending Limb ◽

Diuretic Resistance ◽

First Line Therapy ◽

Advanced Stages

Diuretic drugs are used almost universally in patients with congestive heart failure, most frequently the potent loop diuretics. Despite their unproven effect on survival, their indisputable efficacy in relieving congestive symptoms makes them first line therapy for most patients. In the treatment of more advanced stages of heart failure diuretics may fail to control salt and water retention despite the use of appropriate doses. Diuretic resistance may be caused by decreased renal function and reduced and delayed peak concentrations of loop diuretics in the tubular fluid, but it can also be observed in the absence of these pharmacokinetic abnormalities. When the effect of a short acting diuretic has worn off, postdiuretic salt retention will occur during the rest of the day. Chronic treatment with a loop diuretic results in compensatory hypertrophy of epithelial cells downstream from the thick ascending limb and consequently its diuretic effect will be blunted. Strategies to overcome diuretic resistance include restriction of sodium intake, changes in dose, changes in timing, and combination diuretic therapy. DOI: http://dx.doi.org/10.3329/jdnmch.v17i1.12193 J. Dhaka National Med. Coll. Hos. 2011; 17 (01): 44-46

Download Full-text

Role of renal nerves in control of sodium excretion in chronic congestive heart failure

AJP Renal Physiology ◽

10.1152/ajprenal.1989.256.6.f1084 ◽

1989 ◽

Vol 256 (6) ◽

pp. F1084-F1093 ◽

Cited By ~ 5

Author(s):

H. L. Mizelle ◽

J. E. Hall ◽

J. P. Montani

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Sodium Excretion ◽

Sodium Intake ◽

Left Kidney ◽

Renal Nerves ◽

Chronic Congestive Heart Failure ◽

Control Mechanisms ◽

Sodium Retention ◽

Ventricular Pacing

The aim of this study was to examine the contribution of the renal nerves to the sodium retention in chronic congestive heart failure produced by rapid ventricular pacing. In 10 female dogs the left kidney was denervated and the urinary bladder was split to allow separate 24-h urine collection from an innervated and a denervated kidney in the same dog. The dogs were placed on an 80-meq/day sodium intake and permitted to recover for at least 2 wk. Control measurements were made for 5 days followed by ventricular pacing at 270-300 beats/min for 6 days. Cardiac output (CO), measured with an electromagnetic flow probe around the ascending aorta, fell from a control of 2.4 +/- 0.3 to 1.4 +/- 0.2 l/min (6 day average) during pacing while mean arterial pressure (MAP) fell from 91 +/- 4 to 71 +/- 3 mmHg. In six dogs, sodium excretion fell to an average of less than 2 meq/day (80 meq/day intake) during the 6-day pacing period in both the innervated and denervated kidneys. In four dogs, sodium excretion returned back toward control on days 3-6 of pacing despite sustained reductions in CO and MAP. However, there were no differences in renal hemodynamics or electrolyte excretion between innervated and denervated kidneys in either the compensated or decompensated dogs. These results suggest that other control mechanisms, besides the renal nerves, are primarily responsible for the sodium retention in this model of chronic congestive heart failure.

Download Full-text