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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two cases of acute pulmonary distress following very shortly after irradiation of the upper half of the body are described. The first occurred one hour and forty minutes after irradiation and led to the patient's death three hours after irradiation. The second occurred 15 minutes after irradiation and was successfully treated with hydrocortisone and Frusemide. The features are the sudden onset of dyspnoea and cyanosis associated with pyrexia. Auscultatory evidence of pulmonary oedema was not apparent initially. The response to steroid alone is transitory. High single-dose pulmonary irradiation causes transudation of extracellular fluid and diapedesis of red cells from the alveolar capillaries. The supervention of these effects on severly compromised pulmonary function can well prove dangerous.
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PMID:Acute pulmonary distress following high-dose irradiation of the upper half of the body. 11 68

In human kidney transplantation, a high blood flow established through the graft immediately upon clamp release is usually associated with immediate satisfactory renal function. One hundred consecutive kidney transplant patients were thus provided with a large volume of fluid during surgery. To avoid pulmonary edema, fluid load was given under mean pulmonary arterial pressure (PAP) monitoring, and controlled ventilation was maintained during the early postoperative period. Whether initial PAP value was within normal range or elevated, all patients required an equivalent fluid load to reach the best hemodynamic condition upon clamp removal. The mean intraoperative fluid load consisted of 2406 +/- 968 ml of water with 22.8 +/- 9.4 g of sodium chloride, 5.9 +/- 1.8 units of albumin, and 2.6 +/- 1.8 units of packed red blood cells. Immediately before clamp release patients were given furosemide and mannitol. During the postoperative period, i.v. infusions consisted of water and sodium chloride (6 g/liter) to match urine output, provided that diuresis was equal to or above 400 ml/hr. If diuresis remained or decreased below this level, diuresis replacement was associated with PAP-controlled infusion of saline, albumin, and red blood cells if needed. Furosemide was eventually given if diuresis did not increase above 400 ml/hr with fluid loading. With this protocol a good early diuresis was established in 95% of the cases. Ten patients required dialysis before the 5th postoperative day, one of them because of fluid overload and anuria. Concurrently, a decreased mortality rate and an increased graft survival rate were observed.
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PMID:Early anuria prevention in human kidney transplantation. Advantage of fluid load under pulmonary arterial pressure monitoring during surgical period. 38 63

Furosemide which is claimed to prevent acute mountain sickness and pulmonary oedema of high altitude was tried in experimental animals to evaluate its usefulness or otherwise as a measure of prophylaxis. 90 mice, 128 rats and 44 guinea pigs--all males--were used for the studies. Half the number in each species were kept as controls. The remaining half were further divided into two batches. The first batch was given furosemide 10 mg/kg body weight. Two h later they were exposed to simulated altitude of 30,000 ft for 6 h. The second batch was given two injections of furosemide at intervals of 24 h before exposure to simulated altitude. The controls were given distilled water. Our results show that the death rate was more in the furosemide-treated groups, both under mild as well as severe dehydration in all species. The present study does not substantiate the claim than the drug can be used as prophylactic against acute mountain sickness and pulmonary oedema of high altitude.
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PMID:Effect of furosemide on altitude tolerance in experimental animals. 44 33

For the emergency care of respiratory disorders, in addition to clearing of the airways and keeping them open, drug treatment has an important role to play. The bronchodilatory effect of beta-sympathicomimetics brings about a marked decrease in the resistance to flow, but potential cardiovascular side effects must be considered. In the case of theophylline, the solvent, ethylene diamine has its own pharmacodynamic effects that can make it necessary to select different theophylline preparations. The drugs with a primarily cardiac effect, nitroglycerin, dobutamine and dopamine can produce pulmonary relief. Furosemide is specifically indicated for pulmonary edema. In addition to experience in the use of emergency drugs, an appropriate basic knowledge of the pharmacodynamics and pharmacokinetics is indispensable.
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PMID:[Emergency drugs in respiratory disorders. A choice of commonly used substances]. 168 8

The efficacy of insulin administration in reversing haemodynamic changes in pulmonary oedema in victims of poisonous scorpion sting is assessed by a study based on animal experiments in which insulin administration reversed metabolic and electrocardiographic changes induced by scorpion envenomation. Six previously healthy children aged 18 months to 11 years were admitted to hospital five to 17 hours after scorpion sting. Frusemide for raised central venous pressure and pulmonary oedema, crystalloid infusion for reduced central venous pressure, and hydrocortisone and dopamine for hypotension were used as standard therapy. Insulin (0.3 units g-1 of glucose) was administered when the standard therapy failed to produce an improvement, and at the earliest sign of haemodynamic instability. Reversal of pulmonary oedema and haemodynamic changes, and attainment or normal respiratory rate, blood pressure and central venous pressure, were observed. It is concluded that insulin administration may be useful in reversing haemodynamic changes and pulmonary oedema in victims of scorpion stings.
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PMID:Insulin reverses haemodynamic changes and pulmonary oedema in children stung by the Indian red scorpion Mesobuthus tamulus concanesis, Pocock. 181 42

The possibility of using impedance plethysmography to assess changes in the volume of the extravascular lung fluid in intensive therapy and resuscitation patients is discussed. Changes in the volume of the fluid during extracorporeal detoxication are analysed. A correlation was found between these changes and lung distensibility (r = -0.7). A significant diminution of the fluid volume was observed in response to therapeutic doses of Lasix and Nitroglycerin. Data are cited on the increasing (85 percent) volumes of the fluid in preclinical pulmonary edema in patients with left ventricular insufficiency.
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PMID:[Possibilities of the method of dilution of electro-impedance indicators in the assessment of volume dynamics of extravascular lung fluid in intensive care and resuscitation units]. 212 42

Clinical experience with five patients exposed to phosgene is described. The treatment of phosgene poisoning was focused upon the presenting problem, pulmonary edema. Arterial hypoxemia was treated with a face mask with 10 cm CPAP with the FiO2 adjusted as needed or with a volume ventilator with controlled ventilation. Ventilation was controlled to reduce the work of breathing. Metabolic acidosis was treated with NaCHO3 to produce a normal pH. A vigorous program of diuresis was used to treat the pulmonary edema. Lasix was administered to produce a negative fluid balance while maintaining a good urinary output. The negative fluid balance correlated well with reduced oxygen requirements.
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PMID:Phosgene: a practitioner's viewpoint. 302 27

Previous data suggest that furosemide improves gas exchange in pulmonary edema by preferential perfusion of nonedematous lung units. To test whether this is a direct effect of furosemide on the pulmonary vasculature as opposed to a secondary phenomenon resulting from the known peripheral effects of this drug, the effect of furosemide on the pressure-flow characteristics of the pulmonary vasculature was studied in six isolated perfused canine lungs with different degrees of gravimetrically determined edema. Furosemide shifted the pressure-flow curve by decreasing the mean intercept or average closing pressure of the pulmonary vascular bed from 13.8 +/- 5.3 to 9.5 +/- 5.4 cm H2O and the zero-flow critical closing pressure from 9.3 +/- 4.3 to 4.7 +/- 3.5 cm H2O (P less than 0.05). The slopes of these curves did not change between control and furosemide treatment. The decrease in intercept and the decrease in zero-flow critical closing pressures were closely correlated with the increase in edema (r = 0.895 for average closing pressure and r = -0.928 for critical closing pressure) (P less than 0.05). Furosemide doubled the pulmonary blood flow in the isolated lobe for the same driving pressure and the greater the amount of lobar edema the less pronounced was this furosemide-associated increase in blood flow. This direct effect of furosemide on the pulmonary vasculature could explain the improved gas exchange seen before a decrease in pulmonary edema, since this pulmonary vasoactivity would result in preferential perfusion of nonflooded alveolar units.
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PMID:The effect of lung edema on pulmonary vasoactivity of furosemide. 663 65

Changes in blood volume were investigated following intravenous injection of a single dose of furosemide in 21 patients with pulmonary edema. In a subset of 10 patients in whom the blood urea nitrogen level was 11.4 +/- 2.2 mg/dl and the serum creatinine level was 1.3 +/- 0.1 mg/dl and in whom total urine output exceeded 1 liter over a four- to six-hour interval ("diuretic" group), no significant change in plasma or total blood volume was observed, nor were there any significant changes in hematocrit. In a "nondiuretic" group of 11 patients who had moderately decreased renal function (blood urea nitrogen level 59.3 +/- 13.0 mg/dl and serum creatinine level 2.3 +/- 0.3 mg/dl) and in whom total urine output was less than 1 liter over the four- to six-hour interval, there was a significant increase in blood volume with a concomitant decrease in hematocrit and hemoglobin levels. Furosemide-induced diuresis therefore did not deplete intravascular volume. To the contrary, actions of furosemide that were independent of its diuretic action were associated with an expansion of plasma volume in the absence of diuresis. This may be related to the venous capacitance effects of furosemide with lowering of venous resistance and, therefore, lowering of the capillary hydrostatic pressure. In addition, there was an increase in colloid osmotic pressure. Both mechanisms increase the effective oncotic pressure gradient, which favors reabsorption of extravascular (edema) fluid. It is concluded that intravascular volume was therefore replenished at a rate equal to or in excess of the volume removed by diuresis.
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PMID:Blood volume following diuresis induced by furosemide. 671 72

Effective diuresis requires both sufficient glomerular filtrate and adequate delivery of the diuretic drug to the lumen of the renal tubule. Diuretics will not "force open" the kidney. Diuretics that work primarily in the proximal tubule include osmotic diuretics (e.g., mannitol), diuretics that interfere with the adenyl cyclase system (e.g., xanthines), and those which inhibit carbonic anhydrase (e.g., acetazolamide). Some thiazide and thiazide-like diuretics have a secondary site of action in the proximal tubule based on either carbonic anhydrase inhibition or other mechanisms, such as inhibition of sodium phosphate reabsorption. The diuretics that work primarily in the medullary diluting segment of the loop of Henle, furosemide and ethacrynic acid, block the active reabsorption of chloride and interfere with the tubular reabsorption of free water. The exact mechanism remains unknown. These diuretics tend to have a "high ceiling," to be potent and rapidly acting, and to have a short duration of effect. They are excellent for the treatment of severe fluid overload or pulmonary edema but are not ideal for the treatment of uncomplicated hypertension. Furosemide is a sulfonamide derivative; ethacrynic acid can be used in patients who are allergic to sulfa drugs. Diuretics that work primarily in the cortical diluting segment include the thiazides and thiazide-like drugs. They inhibit sodium transport by an undetermined mechanism. Most of them seem to reach a dose-response plateau beyond which little additional effect is gained by increasing the dose. Most of them appear to lose efficacy as the glomerular filtration rate decreases, except for metolazone and indapamide. The thiazides are most commonly used to treat hypertension. Diuretics that work primarily in the distal tubule and collecting tubule include the aldosterone inhibitor spironolactone and two drugs that impair tubular reabsorption of sodium by direct action, triamterene and amiloride. These drugs are primarily used for their potassium-sparing effect.
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PMID:Insights into intrarenal sites and mechanisms of action of diuretic agents. 686 1


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