Diuretic therapy

Fmit and vegetable juices high in potassium have been recommended to correct hypokalemic alkalosis in patients on diuretic therapy. Apparendy the efficacy of this treatment is questionable. A possible reason for ineffectiveness is the low Ck content of most of these juices. Because Ck is high only in juices in which Na" is high, these have to be excluded (64). 

Diuretics, such as those of the thiazide type, have been the cornerstone of first-line antihypertensive treatments for decades. However, popularity and use have eroded as a result of increases in sudden death in patients on diuretic therapy, and unfavorable effects on blood Hpids profile, ie, increasing cholesterol and triglyceride. These effects have been impHcated as possible causes for the lack of decrease in the mortaUty rate resulting from acute MI in patients treated with a diuretic (187,240,241). However, diuretics do protect against stroke and CHF. 

Hypokalemia. Hypokalemia associated with thia2ide diuretic therapy has been knpHcated in the increased incidence of cardiac arrhythmias and sudden death (82). Several large clinical trials have been conducted in which the effects of antihypertensive dmg therapy on the incidence of cardiovascular complications were studied. The antihypertensive regimen included diuretic therapy as the first dmg in a stepped care (SC) approach to lowering the blood pressure of hypertensive patients. 

When adrninistered long-term for the treatment of hypertension, diuretics fulfill the goals of preventing cardiovascular disease and increasing longevity. However, diuretic therapy may produce both side and toxic effects that are significant in certain patient subgroups, eg, diabetics and cardiac patients. 

Taylor SH (2000) Diuretic therapy in congestive heart failure. Cardiol Rev 8 104-114... 

The ACE inhibitors may cause a significant drop in blood pressure after the first dose This effect can be minimized by discontinuing the diuretic therapy (if the patient is taking a diuretic) or by increasing salt intake for at least 1 week before treatment with the ACE inhibitors is begun or beginning treatment with small doses. After the first dose of an ACE inhibitor, the nurse monitors the blood pressure every 15 to 30 minutes for at least 2 hours and afterward until the blood pressure is stable for 1 hour. 

DISPLAY 46-1 Signs and Symptoms of Cbmmon Fluid and Electrolyte Imbalances Associated With Diuretic Therapy... 

The nurse must closely observe patients receiving a potassium-sparing diuretic for signs of hyperkalemia (see Display 46-1), a serious and potentially fatal electrolyte imbalance The patient is closely monitored for hypokalemia during loop or thiazide diuretic therapy. A supplemental potassium supplement may be prescribed to prevent hypokalemia. The primary health care provider may also encourage the patient to include... 

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

Inadequate diuretic therapy Ineffective cardiac pump function... 

If diuretic therapy is warranted, monitor for therapeutic response by assessing weight loss and improvement of fluid retention, as well as exercise tolerance and presence of fatigue. 

All patients with ascites require counseling on dietary sodium restriction. Salt intake should be limited to less than 800 mg sodium (2 g sodium chloride) per day. More stringent restriction may cause faster mobilization of ascitic fluid, but adherence to such strict limits is very difficult. Patients usually respond well to sodium restriction accompanied by diuretic therapy.14,22,31,32 The goal of therapy is to achieve urinary sodium excretion of at least 78 mEq (78 mmol) per day.22 While a 24-hour urine collection provides this information, a spot urine sodium/ potassium ratio greater than 1.0 provides the same information and is much less cumbersome to perform. 

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. 

Evaluate effectiveness of diuretic therapy with regard to ascitic fluid accumulation and development of peripheral edema. Ask the patient directed questions about abdominal girth, fullness, tenderness, and pain. Weigh the patient at each visit, and ask the patient to keep a weight diary. Assess for peripheral edema at each visit. 

Several adaptive mechanisms by the kidney limit effectiveness of loop diuretic therapy. Postdiuretic sodium retention occurs as the concentration of diuretic in the loop of Henle decreases. This effect can be minimized by decreasing the dosage interval (i.e., dosing more frequently) or by administering a continuous infusion. Continuous infusion loop diuretics may be easier to titrate than bolus dosing, requires less nursing administration time, and may lead to fewer adverse reactions. 

Develop a plan to provide symptomatic care of complications associated with ARF, such as diuretic therapy to treat volume overload. Monitor the patient s weight, urine output, electrolytes (such as potassium), and blood pressure to assess efficacy of the diuretic regimen. 

Diuretic therapy is often necessary to prevent volume overload in patients with CKD. Loop diuretics are most frequently... 

Monitor edema after initiation of diuretic therapy. Monitor fluid intake to ensure obligatory losses are being met and avoid dehydration. If adequate diuresis is not attained with a single agent, consider combination therapy with another diuretic. 

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. 

Potassium is the second most abundant cation in the body and is found primarily in the intracellular fluid. Potassium has many important physiologic functions, including regulation of cell membrane electrical action potential (especially in the myocardium), muscular function, cellular metabolism, and glycogen and protein synthesis. Potassium in PN can be provided as chloride, acetate, and phosphate salts. One millimole of potassium phosphate provides 1.47 mEq of elemental potassium. Generally, the concentration of potassium in peripheral PN (PPN) admixtures should not exceed 80 mEq/L (80 mmol/L). While it is safer to also stick to the 80 mEq/L (80 mmol/L) limit for administration through a central vein, the maximum recommended potassium concentration for infusion via a central vein is 150 mEq/L (150 mmol/L).14 Patients with abnormal potassium losses (e.g., loop or thiazide diuretic therapy) may have higher requirements, and patients with renal failure may require potassium restriction. 

Compensatory mechanisms in HF stimulate excessive sodium and water retention, often leading to systemic and pulmonary congestion. Consequently, diuretic therapy (in addition to sodium restriction) is recommended in all patients with clinical evidence of fluid retention. However, because they do not alter disease progression or prolong survival, they are not considered mandatory therapy for patients without fluid retention. 

The ACC/AHA guidelines recommend use of /1-blockers in all stable patients with HF and a reduced LVEF in the absence of contraindications or a clear history of /Lblocker intolerance. Patients should receive a fi-blocker even if symptoms are mild or well controlled with ACE inhibitor and diuretic therapy, ft is not essential that ACE inhibitor doses be optimized before a /J-blocker is started because the addition of a /J-blocker is likely to be of greater benefit than an increase in ACE inhibitor dose. 

Acutely, diuretics lower BP by causing diuresis. The reduction in plasma volume and stroke volume associated with diuresis decreases cardiac output and, consequently, BP. The initial drop in cardiac output causes a compensatory increase in peripheral vascular resistance. With chronic diuretic therapy, the extracellular fluid volume and plasma volume return almost to pretreatment levels, and peripheral vascular resistance falls below its pretreatment baseline. The reduction in peripheral vascular resistance is responsible for the long-term hypotensive effects. Thiazides lower BP by mobilizing sodium and water from arteriolar walls, which may contribute to decreased peripheral vascular resistance. 

ACE inhibitor with diuretic therapy is recommended as the first-line regimen of choice. ACE inhibitors have numerous outcome data showing reduced CV morbidity and mortality. Diuretics provide symptomatic relief of edema by inducing diuresis. Loop diuretics are often needed, especially in patients with more advanced disease. 

Diuretic therapy should be initiated with single morning doses of spironolactone, 100 mg, and furosemide, 40 mg, with a goal of 0.5-kg maximum daily weight loss. The dose of each can be increased together, maintaining the 100 40 mg ratio, to a maximum daily dose of 400 mg spironolactone and 160 mg furosemide. 

If tense ascites is present, a 4- to 6-L paracentesis should be performed prior to institution of diuretic therapy and salt restriction. 

Patients who experience encephalopathy, severe hyponatremia despite fluid restriction, or renal insufficiency should have diuretic therapy discontinued. 

Nephron adaptation to chronic diuretic therapy NSAID use Heart failure... 

Diuretic therapy or dialysis may be necessary to control edema or blood pressure. 

Patients with hypervolemic hypotonic hyponatremia should be treated with 3% saline and prompt initiation of fluid restriction. Loop diuretic therapy will also likely be required to facilitate urinary excretion of free water. 

Pulmonary edema requires immediate pharmacologic treatment. Other forms of edema can be treated gradually with, in addition to diuretic therapy, sodium restriction and correction of underlying disease state. 

This is not the only example. Recently, polymorphisms in the G protein p3-subunit gene have been shown to predict response to hydrochlorothiazide (Turner et al., 2001). Psaty et al. identified a subset of patients with a variant of the a-adducin gene that were associated with a lower risk of myocardial infarction and cerebral hemorrhage with diuretic therapy (Psaty et al., 2002). In addition, Genaissance has indicated that it has identified markers that predict the response to the statins, a class of drugs used to lower cholesterol. 

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