Congestive cardiac failure

The main account appears in Chapter 24 where the emphasis is now on early use of ACE-inhibitors and other therapies which are specifically diuretic-sparing. Nevertheless, because diuretics by mouth are easily given repeatedly, lack of supervision can result in insidious overtreatment. Relief at disappearance of the congestive features can mask exacerbation of the low output symptoms of heart failure, such as tiredness and postural dizziness due to reduced blood volume. A rising blood urea is usually evidence of reduced glomerular blood flow consequent on a fall in cardiac output, but does not distinguish whether the cause of the reduced output is overdiuresis or worsening of the heart failure itself. The simplest guide to the success or failure of diuretic regimens is to monitor body weight, which the patient can do equipped with just bathroom scales. Fluid intake and output charts are more demanding of nursing time, and often less accurate.

Acute pulmonary oedema: left ventricular failure

(Seep. 518) Renal oedema

The chief therapeutic aims are to reduce dietary sodium intake and to prevent excessive sodium retention using diuretic drugs. Reduction of sodium reabsorption in the renal tubule by diuretics is most effective where glomerular filtration has not been seriously reduced by disease. Frusemide and bumetanide are effective even when the filtration rate is very low; frusemide may usefully be combined with metolazone but the resulting profound diuresis requires careful monitoring. Secondary hyperaldosteronism complicates the nephrotic syndrome because albumin loss causes plasma colloid pressure to fall, and the resulting diversion of intravascular volume to the interstitium activates the renin-angiotensin-aldosterone system; then spironolactone may be added usefully to potentiate a loop diuretic and to conserve potassium, loss of which can be severe.

Hepatic ascites (see also p. 656)

Ascites and oedema are due to portal venous hypertension together with decreased plasma colloid osmotic pressure causing hyperalodosteronism as with nephrotic oedema (above). Furthermore, diversion of renal blood flow from the cortex to the medulla favours sodium retention. In addition to dietary sodium restriction, a loop diuretic plus spironolactone are used to produce a gradual diuresis; too vigorous depletion of sodium with added potassium loss and hypochloraemic alkalosis may cause hepatic coma. Abdominal paracentesis can be very effective if combined with human albumin infusion to prevent further aggravating hypoproteinaemia.

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