Potassium concentrations

The addition of potassium to Fe single crystals also enliances the activity for ammonia synthesis. Figure A3.10.19 shows the effect of surface potassium concentration on the N2 sticking coefficient. There is nearly a 300-fold increase in the sticking coefficient as the potassium concentration reaches -1.5 x 10 K atoms cm ... 

Potassium-sparing by diuretic agents, particularly spironolactone, enhances the effectiveness of other diuretics because the secondary hyperaldosteronism is blocked. This class of diuretics decreases magnesium excretion, eg, amiloride can decrease renal excretion of potassium up to 80%. The most important and dangerous adverse effect of all potassium-sparing diuretics is hyperkalemia, which can be potentially fatal the incidence is about 0.5% (50). Therefore, blood potassium concentrations should be monitored carehiUy. 

Potassium, concentration by use of ion-exchange membrane, 235 determination by x-ray emission spectrography, 222, 328... 

Mild (5.S-6.5 mEq/L) to moderate (6.5-8 mEq/L) potassium blood level increases may be asymptomatic and manifested only by increased serum potassium concentrations and characteristic BOS changes such asdisappearance of P waves or Rereading (widening) of the QRS complex. 

Ponds, Pu distribution coefficients. 299-302 Potassium, concentration in natural... 

Tissue Potassium concentration (mol m ) Cytoplasm Vacuole Reference... 

Leigh, R.A. Wyn Jones, R.G. (1984). A hypothesis relating critical potassium concentrations for growth to the distribution and functions of the ion in the plant cell. New Phytologist, 97, 1-13. 

Weber, L. A., Hickey, E.D., Nuss, D.L. Bayloni, C. (1977). 5 -terminal 7-methyl-guanosine and messenger RNA function influence of potassium concentration on translation in vitro. Journal of Biological Chemistry, 252, 4007-10. 

Serum potassium concentration Is Increased by the concurrent administration of Intravenous potassium penicillin 6. The penicillin preparation contains 1.7 mmol of potassium per million units. Thus, a patient receiving 10 million units of the antibiotic receives 17 mmol (m q.) of potassium. 

However, although high potassium concentration was thought essential in early experimental work (Acquatella etcd., 1972), Fuller and Pe (1976) reported that potassium concentrations much higher than normal plasma levels led to poor renal function. A number of more recent studies have claimed that solutions containing high concentrations of sodium ions were equally or even more effective than those with high potassium (Moen et al., 1989 Sumimoto etal., 1989 Marshall etal., 1991). 

FIG. 15 Time course of the potassium concentration in nitrobenzene containing ( ) no or (O) 1 wt% TDDMA-SCN upon equilibration with 10 M KSCN, as determined by ASS. (From Ref. 16.)... 

The major risk related to aldosterone antagonists is hyperkalemia. Therefore, the decision for use of these agents should balance the benefit of decreasing death and hospitalization from HF and the potential risks of life-threatening hyperkalemia. Before and within one week of initiating therapy, two parameters must be assessed serum potassium and creatinine clearance (or serum creatinine). Aldosterone antagonists should not be initiated in patients with potassium concentrations greater than... 

In patients without contraindications, spironolactone is initiated at a dose of 12.5 to 25 mg daily, or occasionally on alternate days for patients with baseline renal insufficiency. Eplerenone is used at a dose of 25 mg daily, with the option to titrate up to 50 mg daily. Doses should be halved or switched to alternate-day dosing if creatinine clearance falls below 50 mL/minute. Potassium supplementation is often decreased or stopped after aldosterone antagonists are initiated, and patients should be counseled to avoid high-potassium foods. At anytime after initiation of therapy, if potassium concentrations exceed... 

Aldosterone antagonists Hypotension, hyperkalemia, increased serum creatinine BP and HR every shift during oral administration during hospitalization, then once every 6 months baseline SCr and serum potassium concentration SCr and potassium at 48 hours, at 7 days, then monthly for 3 months, then every 3 months thereafter following hospital discharge... 

The ventricular action potential is depicted in Fig. 6-2.2 Myocyte resting membrane potential is usually -70 to -90 mV, due to the action of the sodium-potassium adenosine triphosphatase (ATPase) pump, which maintains relatively high extracellular sodium concentrations and relatively low extracellular potassium concentrations. During each action potential cycle, the potential of the membrane increases to a threshold potential, usually -60 to -80 mV. When the membrane potential reaches this threshold, the fast sodium channels open, allowing sodium ions to rapidly enter the cell. This rapid influx of positive ions... 

Assess possible correctable etiologies, including myocardial ischemia, serum potassium concentration (for hyperkalemia), and thyroid function tests (for hypothyroidism). 

Monitor serum potassium in patients receiving high-dose or continuous nebulization of a short-acting p2-agonist. Serum potassium concentrations should be obtained upon admission, and if hypokalemic, every 4 hours (after each 30 to 40 mEq or mmol of replacement) until the patient s potassium is stable. Potassium should be monitored every 3 to 6 months after discharge. 

As nephron mass decreases, both the distal tubular secretion and GI excretion are increased because of aldosterone stimulation. Functioning nephrons increase FEK up to 100% and GI excretion increases as much as 30% to 70% in CKD,30 as a result of aldosterone secretion in response to increased potassium levels.30 This maintains serum potassium concentrations within the normal range through stages 1 to 4 CKD. Hyperkalemia begins to develop when GFR falls below 20% of normal, when nephron mass and renal potassium secretion is so low that the capacity of the GI tract to excrete potassium has been exceeded.30... 

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... 

Hyperkalemia is defined as a serum potassium concentration greater than 5 mEq/L (5 mmol/L). Manifestations of hyperkalemia include muscle weakness, paresthesias, hypotension, ECG changes (e.g., peaked T waves, shortened QT intervals, and wide QRS complexes), cardiac arrhythmias, and a decreased pH. Causes of hyperkalemia fall into three broad categories (1) increased potassium intake (2) decreased potassium excretion and (3) potassium release from the intracellular space. 

Potassium is the second most abundant cation in the body and is found primarily in the intracellular fluid. Potassium has many important physiologic functions, including regulation of cell membrane electrical action potential (especially in the myocardium), muscular function, cellular metabolism, and glycogen and protein synthesis. Potassium in PN can be provided as chloride, acetate, and phosphate salts. One millimole of potassium phosphate provides 1.47 mEq of elemental potassium. Generally, the concentration of potassium in peripheral PN (PPN) admixtures should not exceed 80 mEq/L (80 mmol/L). While it is safer to also stick to the 80 mEq/L (80 mmol/L) limit for administration through a central vein, the maximum recommended potassium concentration for infusion via a central vein is 150 mEq/L (150 mmol/L).14 Patients with abnormal potassium losses (e.g., loop or thiazide diuretic therapy) may have higher requirements, and patients with renal failure may require potassium restriction. 

Increasing KC1 concentration lowers inhibition as shown in Table II. The fact that damage increased with KC1 concentration is consistant with the ionic ratio hypothesis and suggests a base exchange mechanism whereby calcium ions are more easily extracted from the clay and replaced by potassium ions as the potassium concentration increases. 

Gibb I., Evaluation and assessment of new disposable strip for determination of plasma potassium concentration, J. Clin. Pathol. 1987 40, 298. 

ACE inhibitors decrease aldosterone and can increase serum potassium concentrations. Hyperkalemia occurs primarily in patients with chronic kidney disease or diabetes and in those also taking ARBs, NSAIDs, potassium supplements, or potassium-sparing diuretics. 

Serum potassium concentration is usually maintained in the normal range until the GFR is less than 20 mL/min per 1.73 m2, when mild hyperkalemia is likely to develop. 

Treatment of hyperkalemia depends on the desired rapidity and degree of lowering (Fig. 78-4, Table 78-6). Dialysis is the most rapid way to lower serum potassium concentration. 

Calcium administration rapidly reverses ECG manifestations and arrhythmias, but it does not lower serum potassium concentrations. Calcium is short acting and therefore must be repeated if signs or symptoms recur. 

In contrast to the metabotropic effects described for presynaptic kainate receptors in CA1 (90,94), the effects of kainate in CA3 appear to be mediated by direct depolarization of the presynaptic terminals. The kainate-induced facilitation is not sensitive to antagonists of other receptors (e.g., GABAb), and can be mimicked by elevating the extracellular potassium concentration (77,100). It has been proposed that the facilitation is owing to increased calcium influx that is induced by modest depolarization of the terminals by kainate receptors, whereas a strong depolarization, in response to activation of a larger receptor population, causes the sodium channels to inactivate and thereby depresses transmission (77,84,88,100-102). 

---