Heart failure thiazide

Thiazide diuretics act on the beginning of the distal convoluted tubule by inhibiting sodium re-absorption. Thiazide diuretics are indicated in hypertension, and at higher doses to relieve oedema caused by heart failure. Thiazide diuretics lead to hyponatraemia and hypokalaemia. They may cause hypercalcaemia and are therefore avoided in patients with this condition. 

A 55-year-old patient currently receiving other drugs for another condition is to be started on diuretic therapy for rrald heart failure. Thiazides are known to reduce the excretion of (A) Diazepam Fluoxetine Imipramine Lithium Potassium... 

Thiazides Hypertension, congestive heart failure, renal calcium... 

Therapy of congestive heart failure. By lowering peripheral resistance, diuretics aid the heart in ejecting blood (reduction in afterload, pp. 132, 306) cardiac output and exercise tolerance are increased. Due to the increased excretion of fluid, EEV and venous return decrease (reduction in preload, p. 306). Symptoms of venous congestion, such as ankle edema and hepatic enlargement, subside. The drugs principally used are thiazides (possibly combined with K+-sparing diuretics) and loop diuretics. 

Lithium intoxication can be precipitated by the use of diuretics, particularly thiazides and metola-zone, and ACE inhibitors. NSAIDs can also precipitate lithium toxicity, mainly due to NSAID inhibition of prostaglandin-dependent renal excretion mechanisms. NSAIDs also impair renal function and cause sodium and water retention, effects which can predispose to interactions. Many case reports describe the antagonistic effects of NSAIDs on diuretics and antihypertensive drugs. The combination of triamterene and indomethacin appears particularly hazardous as it may result in acute renal failure. NSAIDs may also interfere with the beneficial effects of diuretics and ACE inhibitors in heart failure. It is not unusual to see patients whose heart failure has deteriorated in spite of increased doses of frusemide who are also concurrently taking an NSAID. 

These potent diuretic agents interact with almost the entire nephron, including Henle s loop (Fig. 7). Their primary effect is probably the inhibition of the active reabsorption of chloride ions, which then leads to the enhanced excretion of sodium ions and water. Plasma volume is reduced as a result of these effects, whereas in the long-term both cardiac preload and afterload will diminish. The metabolic side-effects of the loop diuretics are globally the same as those of the thiazides, with some incidental differences. Plasma renin activity increases by loop diuretic treatment and it can be well imagined that this effect is noxious in the long-term management of heart failure. The loop diuretics provoke a clearly... 

Potassium-sparing diuretics, such as amiloride and triamterene. These agents reduce at the tubular level the reabsorption of sodium and water, whereas the excretion of potassium is diminished. Their primary effects are independent of aldosterone. They are slow-acting and weak diuretics, which are unsuitable as monotherapy of hypertension or heart failure. For this reason, they are always combined with thiazide or loop diuretics. Several combined preparations are commercially available. 

Diuretics (thiazide, Heart failure Gout Pregnancy... 

Captopril, as well as other ACE inhibitors, is indicated in the treatment of hypertension, congestive heart failure, left ventricular dysfunction after a myocardial infarction, and diabetic nephropathy. In the treatment of essential hypertension, captopril is considered first-choice therapy, either alone or in combination with a thiazide diuretic. Decreases in blood pressure are primarily attributed to decreased total peripheral resistance or afterload. An advantage of combining captopril therapy with a conventional thiazide diuretic is that the thiazide-induced hypokalemia is minimized in the presence of ACE inhibition, since there is a marked decrease in angiotensin Il-induced aldosterone release. 

Triamterene can be used in the treatment of congestive heart failure, cirrhosis, and the edema caused by secondary hyperaldosteronism. It is frequently used in combination with other diuretics except spironolactone. Amiloride, but not triamterene, possesses antihypertensive effects that can add to those of the thiazides. 

Thiazides Hydrochlorothiazide Block Na/CI transporter in renal distal convoluted tubule Reduce blood volume plus poorly understood vascular effects Hypertension, mild heart failure ... 

Loop diuretics Furosemide Block Na/K/2CI transporter in renal loop of Henle Like thiazides t greater efficacy Severe hypertension, heart failure See Chapter 15... 

See Table 15-5. The major indications for thiazide diuretics are (1) hypertension, (2) heart failure, (3) nephrolithiasis due to idiopathic hypercalciuria, and (4) nephrogenic diabetes insipidus. Use of the thiazides in each of these conditions is described in Clinical Pharmacology of Diuretic Agents. 

See Table 15-6. Potassium-sparing diuretics are most useful in states of mineralocorticoid excess or hyperaldosteronism (also called aldosteronism), due either to primary hypersecretion (Conn s syndrome, ectopic adrenocorticotropic hormone production) or secondary hyperaldosteronism (evoked by heart failure, hepatic cirrhosis, nephrotic syndrome, or other conditions associated with diminished effective intravascular volume). Use of diuretics such as thiazides or loop agents can cause or exacerbate volume contraction and may cause secondary hyperaldosteronism. In the setting of enhanced mineralocorticoid secretion and excessive delivery of Na+ to distal nephron sites, renal K+ wasting occurs. Potassium-sparing diuretics of either type may be used in this setting to blunt the K+ secretory response. 

The diuretic and mild vasodilator actions of the thiazides are useful in treating virtually all patients with essential hypertension and may be sufficient in many. Loop diuretics are usually reserved for patients with renal insufficiency or heart failure. Moderate restriction of dietary Na+ intake (60-100 mEq/d) has been shown to potentiate the effects of diuretics in essential hypertension and to lessen renal K+ wasting. 

Researchers John Baer, Karl Beyer (1914—1996), James Sprague (1916- ), and Frederick Novello formulate the drug chlorothiazide, the first of the thiazide diuretics. This groundbreaking discovery marked a new era in medicine as the first safe and effective long-term treatment for chronic hypertension and heart failure. 

Potassium-sparing diuretics include amiloride (Midamor) and triamterene (Dyrenium). They are used in the treatment of cirrhosis and congestive heart failure. They may be used in conjunction with thiazide diuretics to offset the potassium loss associated with those medications. 

Sodium removal is the next important step—by dietary salt restriction or a diuretic—especially if edema is present. In mild failure, it is reasonable to start with a thiazide diuretic, switching to more powerful agents as required. Sodium loss causes secondary loss of potassium, which is particularly hazardous if the patient is to be given digitalis. Hypokalemia can be treated with potassium supplementation or through the addition of a potassium-sparing diuretic such as spironolactone. As noted above, spironolactone should probably be considered in all patients with moderate or severe heart failure since it appears to reduce both morbidity and mortality. 

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. 

Adverse effects Thiazide diuretics induce hypokalemia and hyperuricemia in 70% of patients, and hyperglycemia in 10% of patients. Serum potassium levels should be monitored closely in patients who are predisposed to cardiac arrhythmias (particularly individuals with left ventricular hypertrophy, ischemic heart disease, or chronic congestive heart failure) and who are concurrently being treated with both thiazide diuretics and digitalis glycosides (see p. 160). Diuretics should be avoided in the treatment of hypertensive diabetics or patients with hyperlipidemia. 

Chlorothiazide [klor oh THYE a zide], the prototype thiazide diuretic, was the first modern diuretic that was active orally and was capable of affecting the severe edema of cirrhosis and congestive heart failure with a minimum of side effects. Its properties are representative of the thiazide group, although newer derivatives such as hydrochlorothiazide or chlorthalidone are now used more commonly. 

Thiazide diuretics are ineffective once the GFR becomes less than 25 mL/min, and loop diuretics are often used at high doses (e.g. furosemide 500 mg to 1 g daily) to gain an effect. Metolazone is effective when combined with a loop diuretic. Potassium-sparing diuretics such as amiloride are not recommended. Spironolactone is not generally used, but is beneficial in low dose for the treatment of heart failure even in patients on dialysis. Beta-blockers and calcium channel blockers are generally well tolerated. Any ankle swelling with calcium channel blockers must not be confused with fluid overload. 

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