Salt and water retention

Moreover, digitahs has indirect effects on the circulation, which in normal hearts results in a small increase in arterial pressure, peripheral resistance, and cardiac output (114). The effects of digitahs on the circulation of an individual experiencing congestive heart failure are much more dramatic, however. The increased cardiac output, for example, increases renal blood flow which can reheve in part the edema of CHF associated with salt and water retention (114). 

Minoxidil Hirsutism, marked salt and water retention... 

When diuretics are combined with other antihypertensive agents, an additive hypotensive effect is usually observed because of independent mechanisms of action. Furthermore, many nondiuretic antihypertensive agents induce salt and water retention, which is counteracted by concurrent diuretic use. 

Fluid and electrolyte balance Average and large doses of hydrocortisone or cortisone can cause elevation of blood pressure, salt and water retention, and increased excretion of potassium. These effects are less likely to occur with the synthetic derivatives except when used in large doses. 

In therapeutic doses, hydralazine produces little effect on nonvascular smooth muscle or on the heart. Its pharmacological actions are largely confined to vascular smooth muscle and occur predominantly on the arterial side of the circulation venous capacitance is much less affected. Because cardiovascular reflexes and venous capacitance are not affected by hydralazine, postural hypotension is not a clinical concern. Hydralazine treatment does, however, result in an increase in cardiac output. This action is brought about by the combined effects of a reflex increase in sympathetic stimulation of the heart, an increase in plasma renin, and salt and water retention. These effects limit the hypotensive usefulness of hydralazine to such an extent that it is rarely used alone. 

In contrast to the structurally related thiazide diuretics, diazoxide causes renal salt and water retention. However, because the drug is used for short periods only, this is rarely a problem. 

Diuretics are the mainstay of heart failure management and are discussed in detail in Chapter 15. They have no direct effect on cardiac contractility their major mechanism of action in heart failure is to reduce venous pressure and ventricular preload. This results in reduction of salt and water retention and edema and its symptoms. The reduction of cardiac size, which leads to improved pump efficiency, is of major importance in systolic failure. Spironolactone and eplerenone, the aldosterone antagonist diuretics (see Chapter 15), have the additional benefit of decreasing morbidity and mortality in patients with severe heart failure who are also receiving ACE inhibitors and other standard therapy. One possible mechanism for this benefit lies in accumulating evidence that aldosterone may also cause myocardial and vascular fibrosis and baroreceptor dysfunction in addition to its renal effects. 

A common reason for diuretic use is for reduction of peripheral or pulmonary edema that has accumulated as a result of cardiac, renal, or vascular diseases that reduce blood delivery to the kidney. This reduction is sensed as insufficient effective arterial blood volume and leads to salt and water retention and edema formation. Judicious use of diuretics can mobilize this interstitial edema without significant reductions in plasma volume. However, excessive diuretic therapy may lead to further compromise of the effective arterial blood volume with reduction in perfusion of vital organs. Therefore, the use of diuretics to mobilize edema requires careful monitoring of the patient s hemodynamic status and an understanding of the pathophysiology of the underlying illness. 

Although diuretics are often successful as monotherapy, they also play an important role in patients who require multiple drugs to control blood pressure. Diuretics enhance the efficacy of many agents, particularly ACE inhibitors. Patients being treated with powerful vasodilators such as hydralazine or minoxidil usually require simultaneous diuretics because the vasodilators cause significant salt and water retention. 

Costello-Boerrigter LC, Boerrigter G, Burnett JC Jr Revisiting salt and water retention New diuretics, aquaretics, and natriuretics. Med Clin North Am 2003 87 475. [PMID 12693735]... 

The secondary mineralocorticoid activity of glucocorticoids can lead to salt and water retention, which can cause hypertension. Although the detailed mechanisms are as yet uncertain, glucocorticoid-induced hypertension often occurs in elderly patients and is more common in patients with total serum calcium concentrations below the reference range and/or in those with a family history of essential hypertension (SEDA-20, 368 19). 

Salt and water retention mediated by secondary hyperaldosteronism can complicate hydralazine treatment, leading to weight gain and peripheral edema, loss of blood pressure control, and rarely cardiac failure (SED-8, 474). 

For example, because an adequate dose of hydralazine causes a significant decrease in peripheral vascular resistance, there will initially be a drop in mean arterial blood pressure, evoking a strong response in the form of compensatory tachycardia and salt and water retention (Figure 11-5). The result is an increase in cardiac output that is capable of almost completely reversing the effect of hydralazine. The addition of a B-blocker prevents the tachycardia addition of a diuretic (eg, hydrochlorothiazide) prevents the salt and water retention. In effect, all three drugs increase the sensitivity of the cardiovascular system to each other s actions. 

If the underlying disease causes cardiac function to deteriorate despite expansion of plasma volume, the kidney continues to retain salt and water, which then leaks from the vasculature and becomes interstitial or pulmonary edema. At this point, diuretic use becomes necessary to reduce the accumulation of edema, particularly that which is in the lungs. Reduction of pulmonary vascular congestion with diuretics may actually improve oxygenation and thereby improve myocardial function. Edema associated with heart failure is generally managed with loop diuretics. In some instances, salt and water retention may become so severe that a combination of thiazides and loop diuretics is necessary. 

Today, it is well known that the introduction of a chlorine or fluorine atom at the C-9 position of the natural adrenal substances cortisone and hydrocortisone (and of their dehydro-analogues) markedly enhances the anti-inflammatory activity of these agents, and is accompanied by a striking increase in both salt and water retention [14]. These undesirable side effects, which are manifested generally by 9-halo-steroids, preclude their use systemically in the management of disorders that are normally responsive to adrenocortical steroid therapy. 

The long-term control of BP over weeks or months involves the renin-angiotensin system and the kidney, which regulate the salt and water content of the body. Blood volume is a major determinant of BP, and if blood volume increases because of salt and water retention BP also increases. Similarly, salt and water depletion or blood loss causes decrease in both blood volume and pressure. 

In addition an excessive production of some hormones, for example the mineralocorticoids such as aldosterone, can cause salt and water retention, which results in oedema. Blockage of the lymphatic system or damage to lymph vessels, perhaps caused by radiation therapy, can produce a local oedema. 

Q8 Dehydration reduces ECF volume, venous return, cardiac output and BP, leading to both a reflex vasoconstrictor response and to the stimulation of the renin-angiotensin system. Angiotensin stimulates the release of aldosterone from the adrenal cortex, which causes salt and water retention in the distal tubule and collecting ducts of the nephron. The same stimuli release ADH... 

NS AIDs BETA-BLOCKERS 1 hypotensive efficacy of beta-blockers with indometacin, piroxicam, and possibly ibuprofen and naproxen. Other NSAIDs do not seem to show this effect Additive toxic effects on kidney, salt and water retention by NSAIDs. NSAIDs can raise BP by inhibiting the renal synthesis of vasodilating prostaglandins. Uncertain why this effect is specific to these NSAIDs Watch for 1 response to beta-blockers with indometacin, piroxicam, ibuprofen and naproxen... 

NSAIDs NITRATES Hypotensive effects of hydralazine, minoxidil and nitroprusside are antagonized by NSAIDs NSAIDs cause salt and water retention in the kidney and can raise BP due to 1 production of vasodilating renal prostaglandins Monitor BP at least weekly until stable... 

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