What Is the Connection Between Furosemide and Heart Failure?

Furosemide is commonly known as furosemide, a diuretic, suitable for primary and secondary hypertension, especially elderly hypertension or those with concurrent heart failure. It is clinically used for the treatment of heart and renal edema, liver cirrhosis, ascites, and hypotension. Its diuretic effect is rapid and powerful.

Furosemide

Common name for furosemide

Chinese name: furosemide

Chinese alias:

For powerful

Clinically used to treat cardiac

1.

1. May have mild nausea, diarrhea, drug rash, itching,

Injection: 20mg (2ml) each. Tablets: 20mg, 40mg each.

[Efficacy Indications] (1) Edema diseases include congestive heart failure, liver cirrhosis, kidney disease (nephritis, renal disease, and acute and chronic renal failure caused by various reasons), especially when the effect of other diuretics is not good The application of this class of drugs may still be effective. Combined with other drugs to treat acute pulmonary edema and acute brain edema. (2) Hypertension is generally not the drug of choice for the treatment of essential hypertension, but when thiazide drugs are not effective, especially when they are accompanied by renal insufficiency or hypertension crisis, this class of drugs is particularly suitable. (3) Prevention of acute renal failure is used for various reasons leading to insufficient renal blood perfusion, such as dehydration, shock, poisoning, anesthesia accidents, and circulatory insufficiency. When it is applied in time to correct insufficient blood volume, it can reduce acute renal failure. Chance of tubule necrosis. (4) Hyperkalemia and hypercalcemia. (5) Dilute hyponatremia, especially when the blood sodium concentration is less than 120mmol / L. (6) Antidiuretic hormone hypersecretion (SIADH). (7) Acute drug poisoning, such as barbiturate poisoning. [Chemical composition] 2-[(2-furanmethyl) amino] -5- (sulfamoyl) -4-chlorobenzoic acid.

[Pharmacological action] 1 Effect on water and electrolyte excretion. Can increase the excretion of water, sodium, chlorine, potassium, calcium, magnesium, phosphorus, etc. Unlike thiazide diuretics, furosemide and other diuretics have a clear dose-response relationship. With the increase of the dose, the diuretic effect is obviously enhanced, and the drug dosage range is larger. This class of drugs mainly inhibits the active reabsorption of NaCl in the thick wall of renal tubular medullary ridges. As a result, the concentration of Na + and C1- in the luminal fluid increases, while the concentration of Na + and Cl- in the medullary fluid decreases, which reduces the gradient of osmotic pressure. , Renal tubule concentration function declines, resulting in increased excretion of water, Na +, Cl-. As Na + reabsorption decreases, Na + concentration in the distal tubule increases, and Na + -K + and Na + -H + exchanges increase, and K + and H + excretion increases. As for the mechanism of & shy; furosemide inhibiting Cl- reuptake in the thick wall of the ascending branch of the renal tubular pulp, a chlorine pump has been thought to exist in this area, and studies have shown that Na + is associated with Na + -K + ATPase outside the basement membrane in this area. , Cl-paired transport system, furosemide reduces Na +, C1- reresorption by inhibiting the function of this system. In addition, furosemide may still inhibit the reabsorption of Na + and Cl- by proximal tubules and distal tubules, and promote the secretion of K + by distal tubules. Furosemide increases Ca2 + and Mg2 + excretion by inhibiting the reabsorption of Ca2 + and Mg2 + by Heinz thurium. Short-term medication can increase uric acid excretion, while long-term medication can cause hyperuricemia.

2 Effects on hemodynamics. Furosemide can inhibit the activity of prostaglandin degrading enzymes, increase the content of prostaglandin E2, and thus have a vasodilator effect. Dilatation of renal blood vessels, reduction of renal blood vessel resistance, increase of renal blood flow, especially deep renal cortex blood flow, is of great significance in the diuretic effect of furosemide, and it is also the theoretical basis for its prevention of acute renal failure. In addition, unlike other diuretics, diuretics do not decrease the glomerular filtration rate while the renal tubular fluid flow increases, which may be related to the reduction of chlorine flowing through dense plaques, which weakens or blocks the bulb-tube balance. Furosemide can expand the volume of the veins in the lungs, reduce pulmonary capillary permeability, and its diuretic effect reduces the amount of return to the heart and reduces the left ventricular end-diastolic pressure, which is helpful for the treatment of acute left heart failure. Since furosemide can reduce pulmonary capillary permeability, it provides a theoretical basis for the treatment of adult respiratory distress syndrome.

[Drug interactions] 1. Adrenal sugar, mineralocorticoids, adrenocorticotropic hormones and estrogen can reduce the diuretic effect of this drug and increase the chance of electrolyte disturbances, especially hypokalemia.

2 Non-steroidal anti-inflammatory analgesics can reduce the diuretic effect of this drug, and the chance of kidney damage is also increased, which is related to the former inhibiting prostaglandin synthesis and reducing renal blood flow.

3 In combination with sympathomimetic drugs and anticonvulsants, diuretic effect is weakened.

4 When used in combination with clobetin (amtox), the effects of both drugs are enhanced, and muscle soreness and rigidity can occur.

5 In combination with dopamine, the diuretic effect is strengthened.

6 Drinking and alcohol-containing preparations and drugs that can cause blood pressure can enhance the diuretic and hypotensive effects of this drug; combined with barbiturates and anesthetics, it can easily cause orthostatic hypotension.

7 This medicine can reduce the excretion of uric acid and increase the blood uric acid. Therefore, when it is used in combination with drugs for treating gout, the dosage of the latter should be adjusted appropriately.

8 The efficacy of hypoglycemic agents.

9 The effect of reducing anticoagulant drugs and antifibrinolytic drugs is mainly related to the decrease in blood volume after diuresis, the increase of blood coagulation factor concentration, and the improvement of liver blood supply and increased synthesis of coagulation factors in the liver by diuresis.

10 This medicine strengthens the effect of non-depolarizing muscle relaxants, which is related to the decrease of blood potassium.

11 Combined with antibiotics such as amphotericin, cephalosporins, aminoglycosides, renal toxicity and ototoxicity increase, especially when the original kidney is damaged.

12 When combined with antihistamines, ototoxicity increases, and tinnitus, dizziness, and dizziness are easy to occur.

13 The nephrotoxicity with lithium is significantly increased and should be avoided as much as possible.

14 Increased chance of hypochlorine alkalosis in combination with sodium bicarbonate.

[Adverse reactions] Commonly related to water and electrolyte disorders, especially in high doses or long-term applications, such as orthostatic hypotension, shock, hypokalemia, hypochloremia, hypochlorine alkalosis, hyponatremia , Hypocalcemia and related thirst, fatigue, muscle soreness, arrhythmia, etc. Rare people have allergic reactions (including rash, interstitial nephritis, and even cardiac arrest), blurred vision, yellow vision, light sensitivity, dizziness, headache, anorexia, nausea, vomiting, abdominal pain, diarrhea, pancreatitis, muscle rigidity Etc., bone marrow suppression leads to granulocytopenia, thrombocytopenic purpura and aplastic anemia, liver function impairment, finger (toe) paresthesia, hyperglycemia, urinary glucose positive, pre-existing diabetes, and hyperuricemia. Tinnitus and hearing impairment are more common when high-dose intravenous rapid injection (greater than 4 to 15 mg per minute) is mostly temporary, and a few are irreversible, especially when other ototoxic drugs are applied at the same time. In hypercalcemia, it can cause kidney stones. It has been reported that this drug can aggravate idiopathic edema.

[Contraindications] Those who are allergic to sulfa drugs are disabled, and newborns and infants under two months are disabled. Liver and kidney dysfunction is disabled.