Volume depletion diuretics

Assess patient for prerenal azotemia and hold diuretic therapy o Fluid resuscitate if evidence of volume depletion... 

Diuretic pharmacotherapy (strict avoidance of intravascular volume depletion)... 

There is a paucity of clinical trial evidence comparing the benefit of diuretics to other therapies for symptom relief or long-term outcomes. Additionally, excessive preload reduction can lead to a decrease in CO resulting in reflex increase in sympathetic activation, renin release, and the expected consequences of vasoconstriction, tachycardia, and increased myocardial oxygen demand. Careful use of diuretics is recommended to avoid overdiuresis. Monitor serum electrolytes such as potassium, sodium, and magnesium frequently to identify and correct imbalances. Monitor serum creatinine and blood urea nitrogen daily at a minimum to assess volume depletion and renal function. 

The target in treating ascites is to effect a fluid loss of approximately 0.5 L per day.22 Because ascites equilibrates with vascular fluid at a much slower rate than does peripheral edema, aggressive diuresis is associated with intravascular volume depletion and should be avoided unless patients have concomitant peripheral edema. Patients with peripheral edema in addition to ascites may require increasing furosemide doses until euvolemia is achieved intravenous diuretics are often necessary.22 Diuretic therapy in cirrhosis is typically lifelong. 

Patients at increased risk of NSAID-induced gastrointestinal adverse effects (e.g., dyspepsia, peptic ulcer formation, and bleeding) include the elderly, those with peptic ulcer disease, coagulopathy, and patients receiving high doses of concurrent corticosteroids. Nephrotoxicity is more common in the elderly, patients with creatinine clearance values less than 50 mL/minute, and those with volume depletion or on diuretic therapy. NSAIDs should be used with caution in patients with reduced cardiac output due to sodium retention and in patients receiving antihypertensives, warfarin, and lithium. 

Starting doses of ACE inhibitors should be low with slow dose titration. Acute hypotension may occur at the onset of ACE inhibitor therapy, especially in patients who are sodium- or volume-depleted, in heart failure exacerbation, very elderly, or on concurrent vasodilators or diuretics. Patients with these risk factors should start with half the normal dose followed by slow dose titration (e.g., 6-week intervals). 

No unique signs or symptoms are associated with mild to moderate metabolic alkalosis. Some patients complain of symptoms related to the underlying disorder (e.g., muscle weakness with hypokalemia or postural dizziness with volume depletion) or have a history of vomiting, gastric drainage, or diuretic use. 

Diuretics especially loop diuretics, can cause blood volume depletion... 

For patients with possible intravascular volume depletion (eg, patients treated with diuretics, particularly those with impaired renal function), initiate candesartan under close medical supervision and consider administering a lower dose. 

Hypotension/Votume- or salt-depleted patients In patients who are intravascularly volume-depleted (eg, those treated with diuretics), symptomatic hypotension may occur. Correct these conditions prior to administration. 

Older patients with CHF may be faced with multiple therapies of diuretics, ACE inhibitors/angioten-sion II blockers and beta-blockers. This puts them at risk of hypotension, orthostatic hypotension, azo-taemia and electrolyte imbalance. Drugs should be added carefully, starting at low dose and patients should be monitored for volume depletion and changes in serum creatinine and electrolyte concentrations. 

Diuretics, specifically the loop diuretics furose-mide or bumetanide, combined with the thiazide like diuretic metolazone are needed in hypertensive urgencies both to lower blood pressure by removing excess volume and to prevent loss of potency from tendency to cause fluid retention. Volume depletion should be watched in patients on diuretics. 

Hypertension alone or in combination with other CV-antihypertensive-ARBs PO Initially, 16 mg once a day in those who are not volume depleted. Can be given once or twice a day with total daily doses of 8-32 mg. Give lower dosage in those treated with diuretics or with severely impaired renal function. 

Volume depletion of some degree occurs with all diuretics following prolonged use. This can cause problems, such as postural hypotension, in those with poor cardiac function. Volume depletion also causes a fall in glomerular filtration that can trigger homeostatic reflexes such as increased aldosterone and antidiuretic hormone secretion. This contributes to electrolyte disturbances, such as hypokalaemia and metabolic alkalosis. 

Hyponatmemia is common with the thiazides and to a lesser extent with the loop diuretics. It occurs when the osmolality of the urine persistently exceeds that of the fluid intake and is associated with the inability of the kidney to produce a dilute urine. It is not usually severe. The origin is multifactorial and involves unrestricted fluid intake and increased ADH activity due to volume depletion. Co-administration of dipsogenic drugs, such as the tricyclic antidepressants, or those with ADH-like effects, such as chlorpropamide, can exacerbate the problem. There are rare occasions when hyponatraemia (Nan- concentration less than 100 mmol-L-l) can be of sufficient severity to be life threatening. 

Acidosis and alkalosis are infrequent. Metabolic acidosis is a side effect of acetazolamide therapy and is due to bicarbonate loss in the PCT. All the K+-sparing diuretics can cause metabolic acidosis by H+ retention in the cells of the collecting duct. Metabolic alkalosis is associated with the loop and thiazide drugs. Reflex responses to volume depletion cause reabsorption of HCO-3 in the PCT and H+ secretion in the collecting tubule. 

Loop diuretics are useful in treating toxic ingestions of bromide, fluoride, and iodide, which are reabsorbed in the TAL. Saline solution must be administered to replace urinary losses of Na+ and to provide , so as to avoid extracellular fluid volume depletion. 

Because Henle s loop is indirectly responsible for water reabsorption by the downstream collecting duct, loop diuretics can cause severe dehydration. Hyponatremia is less common than with the thiazides (see below), but patients who increase water intake in response to hypovolemia-induced thirst can become severely hyponatremic with loop agents. Loop agents are sometimes used for their calciuric effect, but hypercalcemia can occur in volume-depleted patients who have another—previously occult—cause for... 

Thiazides inhibit NaCI reabsorption from the luminal side of epithelial cells in the DCT by blocking the Na+/Q transporter (NCC). In contrast to the situation in the TAL, in which loop diuretics inhibit Ca2+ reabsorption, thiazides actually enhance Ca2+ reabsorption. This enhancement has been postulated to result from effects in both the proximal and distal convoluted tubules. In the proximal tubule, thiazide-induced volume depletion leads to enhanced Na+ and passive Ca2+ reabsorption. In the DCT, lowering of intracellular Na+ by thiazide-induced blockade of Na+ entry enhances Na+/Ca2+ exchange in the basolateral membrane (Figure 15-4), and increases overall reabsorption of Ca2+. Although thiazides rarely cause hypercalcemia as the result of this enhanced reabsorption, they can unmask hypercalcemia due to other causes (eg, hyperparathyroidism, carcinoma, sarcoidosis). Thiazides are useful in the treatment of kidney stones caused by hypercalciuria. 

Hypercalcemia can be a medical emergency. Because loop diuretics reduce Ca2+ reabsorption significantly, they can be quite effective in promoting Ca2+ diuresis. However, loop diuretics alone can cause marked volume contraction. If this occurs, loop diuretics are ineffective (and potentially counterproductive) because Ca2+ reabsorption in the proximal tubule would be enhanced. Thus, saline must be administered simultaneously with loop diuretics if an effective Ca2+ diuresis is to be maintained. The usual approach is to infuse normal saline and furosemide (80-120 mg) intravenously. Once the diuresis begins, the rate of saline infusion can be matched with the urine flow rate to avoid volume depletion. Potassium chloride may be added to the saline infusion as needed. 

By the very nature of their action, diuretics are often associated with disturbances in fluid and electrolyte balance. Volume depletion, hyponatremia, hypokalemia, and altered pH balance are among the most fre-... 

Therapeutic uses Thiazide diuretics decrease blood pressure in both the supine and standing positions postural hypotension is rarely observed, except in elderly, volume-depleted patients. These agents counteract the sodium and water retention observed with other agents used in the treatment of hypertension (for example, hydralazine). Thiazides are therefore useful in combination therapy with a variety of other antihypertensive agents including (3-blockers and ACE inhibitors. Thiazide diuretics are particularly useful in the treatment of black or elderly patients, and in those with chronic renal disease. Thiazide diuretics are not effective in patients with inadequate kidney function (creatinine clearance less than 50 mls/min). Loop diuretics may be required in these patients. 

In addition to spironolactone, ascites can be managed by paracentesis. That is the removal ( tapping ) of ascitic fluid from the peritoneal cavity under aseptic conditions. A colloid (human albumin solution (20%)) is infused (40 mL (8 g of albumin) per litre of ascites drained) intravenously during paracentesis, in order to prevent intravascular volume depletion and the onset of renal failure. Following paracentesis, ascites recurs in the majority (93%) if diuretic therapy is not reinstituted, but recurs in only 18% of patients treated with... 

For weight reduction, e.g. boxers, jockeys diuretics. These are also used to flush out other drugs in the hope of escaping detection severe volume depletion can cause venous thrombosis and pulmonary embolism. 

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