Cardiac failure diuretics

In chronic cardiac failure, diuretics and nitrates reduce preload and provide symptomatic relief without affecting outcome. 

ACE inhibitors are approved for the treatment of hypertension and cardiac failure [5]. For cardiac failure, many studies have demonstrated increased survival rates independently of the initial degree of failure. They effectively decrease work load of the heart as well as cardiac hypertrophy and relieve the patients symptoms. In contrast to previous assumptions, ACE inhibitors do not inhibit aldosterone production on a long-term scale sufficiently. Correspondingly, additional inhibition of aldosterone effects significantly reduces cardiac failure and increases survival even further in patients already receiving diuretics and ACE inhibitors. This can be achieved by coadministration of spironolactone, which inhibits binding of aldosterone to its receptor. 

Undesired effects. The magnitude of the antihypertensive effect of ACE inhibitors depends on the functional state of the RAA system. When the latter has been activated by loss of electrolytes and water (resulting from treatment with diuretic drugs), cardiac failure, or renal arterial stenosis, administration of ACE inhibitors may initially cause an excessive fall in blood pressure. In renal arterial stenosis, the RAA system may be needed for maintaining renal function and ACE inhibitors may precipitate renal failure. Dry cough is a fairly frequent side effect, possibly caused by reduced inactivation of kinins in the bronchial mucosa. Rarely, disturbances of taste sensation, exanthema, neutropenia, proteinuria, and angioneurotic edema may occur. In most cases, ACE inhibitors are well tolerated and effective. Newer analogues include lisinopril, perindo-pril, ramipril, quinapril, fosinopril, benazepril, cilazapril, and trandolapril. 

Thiazide diuretics (benzothiadia-zines) include hydrochlorothiazide, benzthiazide, trichlormethiazide, and cyclothiazide. A long-acting analogue is chlorthalidone. These drugs affect the intermediate segment of the distal tubules, where they inhibit a Na+/Ch cotransport, Thus, reabsorption of NaQ and water is inhibited. Renal excretion of Ca decreases, that of Mg + increases. Indications are hypertension, cardiac failure, and mobilization of edema. 

Fluid overload occurs commonly in patients with renal failure, often in the absence of associated heart disease. If salt and water intake is not controlled in the patient who is oliguric or anaemic, plasma volume and symptoms of congestive heart failure ensue. Hypertension and coronary heart disease with increasing age contributes to the congestive heart failure. Diuretics like loop-diuretics or metolazone may be of value. Digitalis should be used with caution in patients on dialysis as cardiac arrhythmias may ensue in patients receiving dialysis in the presence of hypokalemia. 

Most patients with BN can be effectively treated as outpatients. Medical hospitalizations result from consequences of purging activities, such as frequent vomiting and abuse of laxatives and diuretics, which can create electrolyte imbalances and dehydration. These patients are at risk for developing cardiac arrhythmias due to hypokalemia. If the patient s serum potassium falls below 2.5 mEq/T, the patient should be hospitalized. Other medical emergencies are gastric dilatation and esophageal tears (both are rare). Cardiac failure caused by cardiomyopathy from ipecac intoxication is a medical emergency. 

The sites of action within the kidney and the pharmacokinetics of various diuretic drugs are discussed in Chapter 15. Thiazide diuretics are appropriate for most patients with mild or moderate hypertension and normal renal and cardiac function. More powerful diuretics (eg, those acting on the loop of Henle) such as furosemide are necessary in severe hypertension, when multiple drugs with sodium-retaining properties are used in renal insufficiency, when glomerular filtration rate is less than 30 or 40 mL/min and in cardiac failure or cirrhosis, in which sodium retention is marked. 

Thiazide diuretics are useful in early cardiac failure as they are relatively mild diuretics which can mobilize the oedema. Increasing the dosage of a thiazide above the recommended dose would elicit more side effects without markedly improving therapeutic effects. Changing to a more powerful agent from a different diuretic class is preferable if the patient s condition deteriorates. 

Cardiac failure (See also chapter 25). There is now dear evidence from prospective trials that P-blockade is beneficial in terms of mortality for patients with aU grades of moderate heart failure. Data support the use of both nonselective (carvedilol, a-blocker as well) and Pj-selective (metoprolol and bisoprolol) agents. The survival benefit exceeds that provided by ACE inhibitors over placebo. The negative inotropic effects can still be significant, so the starting dose is low (e.g. bisoprolol 1.25 mg p.o. or carvedilol 3.625 mg b.d.) and may be tolerated only with additional anti-failure therapy e.g. diuretic. 

A test dose should be given to patients who are in cardiac failure (or who are already taking a diuretic for another reason, e.g. hypertension). Maintenance of blood pressure in such individuals may depend greatly on an activated renin-angiotensin-aldosterone system and a standard dose of an ACE inhibitor can cause a catastrophic fall in blood pressure. Except for captopril, most ACE inhibitors (including enalapril) are prodrugs, which are inactive for several hours after dosing. This has favoured the use of captopril... 

Spironolactone. Plasma aldosterone is elevated in heart failure. Spironolactone acts as a diuretic by competitively blocking the aldosterone-receptor, but in addition it has a powerful effect on outcome in cardiac failure (see below). 

Hypokalaemia during diuretic therapy is also more likely in hyperaldosteronism, whether primary or more conunonly secondary to severe liver disease, congestive cardiac failure or nephrotic syndrome. 

Spironolactone (see p. 534) is a competitive aldosterone antagonist which also blocks the mineralocorticoid effect of other steroids it is used in the treatment of primary hyperaldosteronism and as a diuretic, principally when severe oedema is due to secondary hyperaldosteronism, e.g. cirrhosis, congestive cardiac failure. 

A 64-year-old woman with systemic lupus erythematosus took chloroquine for 7 years (cumulative dose 1000 g). She developed sjmcope, and the electrocardiogram showed complete heart block a permanent pacemaker was inserted. The next year she presented with biventricular cardiac failure, skin hyperpigmentation, proximal muscle weakness, and chloroquine retinopathy. Coronary angiography was normal. An echocardiogram showed a restrictive cardiomyopathy. A skeletal muscle biopsy was characteristic of chloroquine myopathy. Chloroquine was withdrawn and she improved rapidly with diuretic therapy. 

In heart failure, depletion of potassium can provoke fatigue and lethargy and can cause ventricular dysrhythmias in the failing heart (102). Potassium depletion can occur in cardiac failure when neurohumoral systems are stimulated by diuretics and can be especially profound when skeletal muscle wasting is advanced (101). However, since heart failure itself, independent of diuretic treatment, is associated with loss of total body potassium, it is difficult to assess the independent contribution of diuretic treatment to this potassium deficit. 

When it is used in cardiac failure, furosemide acts in two ways besides its diuretic effect it produces an immediate fall in left ventricular filhng pressure, which is independent of and precedes diuresis. If furosemide is given intravenously in stable chronic heart failure (which it normally is not), this can be an unwanted effect, causing deterioration (SEDA-11, 199), particularly in patients with pure right ventricular failure. 

Diuretics Indometacin Reduction in natriuretic and diuretic effects can exacerbate congestive cardiac failure Avoid NSAIDs in patients with cardiac failure use sulindac monitor clinical signs of fluid retention... 

A 73-year-old man who had taken pergolide 1.5 mg/day for 4 months developed dyspnea, bilateral pleural effusions, and severe edema of the legs up to the scrotum (5). There was no pleural thickening or any evidence of cardiac failure or nephrotic syndrome. These chnical features were resistant to diuretic therapy but resolved completely within a month of withdrawal of pergohde. The mechanism of this type of very rare reaction is totally unknown. 

Spironolactone has been used as a potassium-sparing diuretic in cardiac failure and in the management of ascites and edema associated with hepatic cirrhosis with secondary hyperaldosteronism. It is also used to treat hyperaldosteronism due to adrenal tumors or adrenal hyperplasia. It has a weak positive inotropic effect and a modest antihypertensive effect, in keeping with its natriuretic action. 

Structural chemists and kidney physiologists responsible for chlorothiazide development for the control of high blood pressure and of edema associated with cardiac failure. Thiazidic compounds and furosemide, another sulfonylurea-derived diuretic, are now universally accepted as a primary treatment for hypertension. 

Avoid cardiac failure secondary to aggressive rehydration. Parenteral rehydration should be avoided at all costs and only used if the child is in shock. Avoid diuretics during the first 1-5 days even if edema is evident. 

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