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Hyponatremia or hyponatraemia is a low concentration of sodium in the blood. [4] It is generally defined as a sodium concentration of less than 135 mmol/L (135 mEq/L), with severe hyponatremia being below 120 mEq/L. [3] [8] Symptoms can be absent, mild or severe.
Pseudohyponatremia is a false low sodium reading that can be caused by high levels of fats or proteins in the blood. [14] [3] Dilutional hyponatremia can happen in diabetics as high glucose levels pull water into the blood stream causing the sodium concentration to be lower.
Doing so lessens the chance of increaseing the serum sodium level too rapidly as blood volume rises and ADH levels fall. [citation needed] In people who are volume depleted (e.g., their blood volume is too low), ADH secretion is increased since volume depletion is a potent stimulus for ADH secretion.
Hypoaldosteronism causes low sodium (hyponatremia), high potassium (hyperkalemia), and metabolic acidosis, a condition in which the body produces excess acid.These conditions are responsible for the symptoms of hypoaldosteronism, which include muscle weakness, nausea, palpitations, irregular heartbeat, and abnormal blood pressure.
Hypernatremia is generally defined as a serum sodium level of more than 145 mmol/L. [3] Severe symptoms typically only occur when levels are above 160 mmol/L. [1] Hypernatremia is typically classified by a person's fluid status into low volume , normal volume, and high volume . [ 1 ]
But many people are on low-sodium, heart-healthy diets due to chronic medical conditions such as high blood pressure, heart, or kidney problems. That's why the American Heart Association ...
EAH is categorized by having a blood serum or plasma sodium level below normal, which is less than 135 mmol/L. [1] Asymptomatic EAH is not normally detected unless the athlete has had a sodium blood serum or plasma test. [1] Hyponatremic encephalopathy may be detected using brain imaging studies and pulmonary edema may be confirmed by x-ray.
All three patients were unable to prevent urinary sodium loss despite low serum sodium levels and no evidence of extrarenal sodium loss. Their hyponatremia responded to salt therapy. They postulated that this provided evidence of an extra-pituitary cerebral structure mediating normal sodium metabolism but were unsure of its location or ...