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Results for “Edema, Cardiac”

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At least 19 recordsLinked to original sources
PubMed1986

An evaluation of ultrafiltration as treatment of therapy-resistant cardiac edema.

In six patients with therapy-resistant cardiac edema, ultrafiltration on two consecutive days removed on an average 7750 ml fluid and reduced body weight by 7.3 kg. A difference between the mean ultrafiltration rate (17.4 ml/min) and the calculated plasma refilling rate (12.7 ml/min) led to a reduction in plasma volume during treatment together with an increase in plasma colloid osmotic pressure. Systemic blood pressure, heart rate and cardiac output were unchanged during ultrafiltration while systemic vascular resistance increased and pulmonary capillary wedge pressure and right atrial pressure decreased significantly. No complications were recorded during or after treatment. Ultrafiltration is a safe method of fluid removal in patients with therapy-resistant cardiac edema and can be used as preparation for cardiac catheterization or surgery.

Adult↗
PubMed1969

Diuretics in cardiac edema--1969.

New and powerful diuretics have made it possible for the physician to control cardiac edema in most patients. At the same time their potentially dangerous side effects make it mandatory for the physician to be knowledgeable and judicious in their use. The appreciation of a few simplified facts about cardiac edema and renal reabsorption of sodium makes the clinical pharmacology of the diuretics much easier to understand, remember and apply.

Benzothiadiazines↗
PubMed1979

Cardiac edema in dogs: distribution of renal blood flow and glomerular filtrate.

The injection of Freund's adjuvant into the pericardial sac of 29 dogs resulted in chronic pericardial tamponade with persistent sodium retention. Micropuncture, clearance, and radioactive microsphere experiments were initiated 6--13 days after pericardial injection and 60 min after pericardiocentesis. Pericardiocentesis increased sodium excretion (from 12.2 to 41.3 microequiv./min) and mean arterial pressure (+ 20 mmHg (1 mmHg = 133.322 Pa)). Central venous pressure decreased 6.5 mmHg, as did hematocrit (from 45.7 to 39.8%) and plasma protein concentration (from 5.88 to 5.15 g%). Pericardiocentesis had no significant effect on renal blood flow (RBF), nor plasma flow. Redistribution of glomerular filtrate was suggested by the observation that superficial nephron glomerular filtration rate increased (from 91 to 108 nL/min) while glomerular filtration rate remained unaltered. Determination of intrarenal distribution of RBF revealed that cortical blood flow also distributed superficially. A significant increase in the fraction of RBF perfusing zone 1 (outer cortex) and a decrease in fractional perfusion of zones 2, 3 and 4 (juxtamedullary cortex) were observed in each experiment following pericardiocentesis. RBF distribution examined in a series of six animals prior to and during the development of pericardial tamponade showed the opposite effect. These results indicate that pericardiocentesis causes redistribution of both glomerular filtrate and RBF to superficial nephrons. The development of pericardial tamponade was associated with increased fractional juxtamedullary blood flow. These changes may have been the result of altered blood pressure, hematocrit, plasma protein concentration, or altered renal resistance.

Animals↗