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Total body potassium

The body s normal daily potassium requirement is 0.5 to 1 mEq/kg (0.5 to 1 mmol/kg) or 40 to 80 mEq (40 to 80 mmol) to maintain a serum potassium concentration of 3.5 to 5 mEq/L (3.5 to 5 mmol/L). Potassium is the most abundant cation in the ICF, balancing the sodium contained in the ECF and maintaining electroneutrality of bodily fluids. Because the majority of potassium is intracellular, serum potassium concentration is not a good measure of total body potassium however, clinical manifestations of potassium disorders correlate well with serum potassium. The acid-base balance of the body affects serum potassium concentrations. Hyperkalemia is routinely seen in... [Pg.410]

Hypokalemia results from a total body potassium deficit or shifting of serum potassium into the intracellular compartment. [Pg.904]

Furosemide rarely causes the syndrome of inappropriate antidiuretic hormone secretion (SIADH) (although it has been found useful in treating some patients with SIADH who cannot tolerate water restriction (428)). In furosemide-induced cases (SEDA-7, 246), serum ADH concentrations were raised, total body sodium was normal, total body potassium greatly reduced, and intracellular water raised at the expense of extracellular fluid volume. However, such cases are rare, and no new cases have been published since this complication was reported in SEDA-7. [Pg.603]

Of electrolyte disturbances that alter the response to a cardiac glycoside, hypokalemia is the most important. It has been estimated that a fall in plasma potassium concentration from 3.5 to 3.0 mmol/1 is associated with a 50% increase in sensitivity to digoxin (144). Total body potassium depletion, even in the absence of hypokalemia, has a similar effect (147). [Pg.656]

In heart failure, depletion of potassium can provoke fatigue and lethargy and can cause ventricular dysrhythmias in the failing heart (102). Potassium depletion can occur in cardiac failure when neurohumoral systems are stimulated by diuretics and can be especially profound when skeletal muscle wasting is advanced (101). However, since heart failure itself, independent of diuretic treatment, is associated with loss of total body potassium, it is difficult to assess the independent contribution of diuretic treatment to this potassium deficit. [Pg.1160]

The thiazides increase potassium excretion, but rarely to such an extent that total body potassium stores are appreciably affected. In most patients there is no reason to think... [Pg.3376]

The total body potassium of a 70 kg subject is 3.5 mol (40 to 59 mmol/kg) of which only 1.5% to 2% is present in the ECF. Nevertheless, plasma K is a relatively good indicator of total K stores with only a few exceptions. Because extracellular concentrations are maintained at the expense of the intracellular supply, plasma concentration can initially be normal and belie a total body deficit of up to 200 mmol. [Pg.1754]

Monitor potassium carefully to avoid hyperkalemia because total body potassium is normal A... [Pg.295]

Conversely, metabolic alkalosis results in hypokalemia as a result of a net loss of hydrogen ion in the serum. In response, the body releases intracellular hydrogen ion into the serum to increase the acidity of the blood in exchange for extracellular potassium ions. This creates a relative deficiency of serum potassium. Serum potassium falls approximately 0.6 mEq/L for each 0.1 unit rise in blood pH. Similarly, this is frequently termed false hypokalemia because there isn t a true deficiency in total body potassium. [Pg.968]

Hypokalemia results when there is a total body potassium deficit, or when serum potassium is shifted into the intracellular compartment. Total body deficits occur in the setting of poor dietary intake of potassium, or when there are excessive renal and gastrointestinal losses of potassium from the body. [Pg.968]

A general rule for potassium replacement is that for every 1 -mEq/L fall of potassium below 3.5 mEq/L, there is a corresponding total body potassium deficit of 100 to 400 mEq. Due to the wide variance in projected deficits each patient s therapy must be individualized and adjustments made on the basis of the patients signs, symptoms, and frequent measurements of serum potassium. In patients receiving loop or thiazide diuretics, 40 to 100 mEq of potassium is generally needed to correct mild deficits. Doses up to 120 mEq may be required in more severe deficiencies. The total daily dose should be divided... [Pg.970]

The total body potassium of the average 70 kg man is approximately 3600 mmol. Almost all is insidecclls(Fig. I). Potassium intake is variable. 30-100 mmol/day in the UK. but much higher in other countries. Potassium losses are equally variable. The kidney excretes the hulk of ingested potassium. Urinary potassium excretion rises in response to increased intake. Potassium excretion by the kidney is primarily dependent upon glomerular filtration. The most important factor which regulates potassium excretion in the urine is the plasma potassium concentration. [Pg.87]

Serum potassium concentrations say little about the total body potassium content, although in practice where acid-base status is normal, hypokalaemic patients are usually potassium depleted. [Pg.87]

Renal failure. The kidneys may not be able to excrete a potassium load when the glomerular filtration rate is very low. The acidosis associated with renal failure contributes to the problem. Mineralocorticoiil dejidency. This is most frequently seen in. Addi.son s Disea.se or in patients receiving aldosterone antagonists. In these patients there is an increase in the total body potassium. [Pg.87]

Intravenous fluids nomially come in units of. itK) ml. Estimated losses and deficits are only rough guides. It is rarely possible to make a closer estimate than 5(K) ml of water and 75 mmol of sixlium. Potassium deficits cannot be accurately measured. However, if a patient has a clinically apparent potassium deficit in the absence of an acid-base disturbance, then the total body potassium loss will be in excess of 5fX) mmol. [Pg.90]

The ion-selective electrode is the basis of instruments that are used for the rapid determination of potassium during surgical procedures or the subsequent recovery. This method is relatively cheap and convenient to use at the patienfs bedside and, in comparison with reference methods, is both accurate and reproducible. The direct potentio-metric determination of potassium (and sodium) in small blood samples is also possible this is a useful development of micro-analytical techniques. The naturally occurring radioactive isotope °K is used to measure total body potassium (Schmidt 1992, Birch and Padgham 1993). [Pg.522]

Pierson RN Jr, Lin DHYand Robert PA (1974) Total-body potassium in health effects of age, sex, height, and fat. Am J Physiol 226 206—212. [Pg.545]

A) Quinidine toxicity caused by inhibition of quinidine metabohsm by the thiazide Direct effects of hydrochlorothiazide on the pacemaker of the heart Thiazide toxicity caused by the effects of quinidine on the kidneys Block of calcium current by the combination of quinidine plus thiazide Reduction of serum potassium caused by the diuretic action of hydrochlorothiazide An important therapeutic or toxic effect of loop diuretics is (A) Decreased blood volume Decreased heart rate Increased serum sodium Increased total body potassium Metabolic acidosis... [Pg.565]

Hypokalemia does not usually require treatment, since it is transient and does not reflect a total body potassium deficit. [Pg.135]

In humans, nine subjects had RbCl administered orally until 10-15% of their total body potassium had been replaced. No toxic effects were reported [52]. [Pg.545]

Isotope dilution bility of total body water, total body potassium, total body electrical conductivity, and dualenergy X-ray absorptiometry Expensive and needs specialized equipment mineral content, fat mass, and lean body mass Noninvasive, safe... [Pg.108]

It is a weak y-emitter, and therefore total body potassium can be determined by measuring the y-radiation of the appropriate wavelength emitted by the body. This requires total enclosure in a shielded whole-body counter for about 15 minutes to achieve adequate precision, and because of this, and the cost of the equipment required, this is again purely a research technique. [Pg.177]

Potassium constitutes about 5% of the mineral content of the body. It is the primary cation of intracellular (within the cells) fluids. Approximately 98% of the total body potassium is located intracellularly, where its concentration is 30 or more times that of the extracellular (between cells) fluid. The concentration of sodium in blood plasma is much higher than potassium. On the other hand, the potassium concentration in muscle tissue and milk is many times higher than sodium. [Pg.872]

TOXICITY. Acute toxicity from potassium (known as hyperpotassemia or hyperkalemia) will result from sudden increases of potassium to levels of about 18 g per day for an adult, provided the kidneys are not functioning properly and there is not an immediate and sharply increased loss of potassium from the body. Although no significant increase in intracellular potassium content or in total body potassium occurs in this condition, hyperkalemia may prove fatal due to cardiac arrest. [Pg.873]


See other pages where Total body potassium is mentioned: [Pg.412]    [Pg.356]    [Pg.235]    [Pg.500]    [Pg.501]    [Pg.967]    [Pg.968]    [Pg.89]    [Pg.92]    [Pg.560]    [Pg.117]    [Pg.124]    [Pg.36]    [Pg.544]   
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