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Palatability comparison of oral potassium chloride solutions.

The palatability of various commercially available potassium chloride preparations was studies. Twenty potassium chloride samples were tested by 152 people from February 1975 to April 1975. Nine samples were placed into a "most preferred" group and divided into 36 possible pairs, each to be tested four times. Twenty-four volunteers tested six pairs of samples and chose the preferred sample in each pair. The three samples, which finished with the highest scores (K-Lyte/Cl Packets, Kato Powder Packets and Kaochlor 10%), although not significantly different from the rest of the subgroup of nine, were all highly flavored and among the most expensive. It is suggested that when selecting a potassium chloride preparation, cost, convenience, palatability, and most importantly, long-term compliance with the prescribed regimen, must be considered.

Administration, Oral↗

Hyperkalemia associated with potassium chloride administration in a cat.

Addition of appropriate amounts of potassium chloride solution to fluid administered i.v. resulted in hyperkalemia in a cat. To evaluate whether incomplete mixing of potassium chloride in the fluid might have resulted in the observed hyperkalemia, 40 mEq (20 ml) of potassium chloride solution was injected into each of three 1-L vinyl bags of 5% dextrose in water, with or without attempting to mix the additive with the fluid in the bag. Measurement of potassium concentrations in the bags revealed that injecting potassium chloride solution into a bag of fluid while that fluid is being administered can result in incomplete mixing and discharge of concentrated potassium chloride from the administration set. The greatest potassium concentration measured in fluid sampled from the administration set was 194 mEq/L.

Animals↗

Potassium chloride: absorption and excretion.

The absorption of potassium chloride in liquid form has been studied, using urinary excretion as an index of absorption. The excretion of potassium chloride was observed after inducing a water diuresis and administering a single dose in liquid form. There is evidence that potassium chloride in liquid form is absorbed rapidly, probably from the stomach, and hence there is a good rationale for its use where rapid absorption is needed, as in digitalis intoxication.

Absorption↗

Formation of thiosulfate [35S] by neutron irradiation of potassium chloride and preparation of elementary sulfur [35S].

Potassium chloride was subjected to various kinds of pretreatments and irradiated in a nuclear reactor. Irradiated potassium chloride was dissolved in deaerated aqueous solution of several sulfur-salts. A portion of the solution was chromatographed on a thin layer chromatographic plate and the distribution of 35S-chemical species was determined. Irradiation of potassium chloride degassed at 3x10(-4)Torr resulted in the formation of about 60% of 35S in the form of thiosulfate and remainder was distributed among sulfide, sulfate and elementary sulfur. Thiosulfate[35S] was converted to elementary sulfur[35S] first by reducing to hydrogen sulfide [35S] with nascent hydrogen and then by oxidizing the latter to elementary sulfur[35S] with hexacyanoferrate(III). Elementary sulfur[35S] was finally extracted into benzene. Radiochemically pure elementary sulfur[35S] could be produced by simple procedures with a yield of about 60%. Thiosulfate[35S] was decomposed with acid to elementary sulfur[35S] and sulfur[35S] dioxide. The former was separated by centrifuging and dispersed in boiling water to form colloidal suspension of elementary sulfur[35S]. Approximately 40% of 35S was recovered as colloid.

Chemical Phenomena↗

Preventing adverse events in the pediatric intensive care unit: prospectively targeting factors that lead to intravenous potassium chloride order errors.

OBJECTIVE: To prospectively identify and reduce proximal causes of error contributing to inappropriate intravenous potassium chloride orders and reduce adverse events subsequent to these ordering errors. DESIGN: Pre-post cohort study of the reduction in both proximal causes of error and number of postinfusion elevated serum potassium levels after intervention. SETTING: Sixteen-bed, tertiary care, urban, academic pediatric intensive care unit. PATIENTS: Children 0-18 yrs old receiving intravenous potassium chloride in the pediatric intensive care unit. INTERVENTIONS: A multidisciplinary team determined proximal causes of error that were likely contributors to the occurrence of the outcome measure, elevated potassium levels after intravenous potassium chloride. A mandatory drug request form was designed for physicians ordering intravenous potassium chloride. The drug request form was designed to reduce proximal causes of error and, as a result, elevated potassium levels after intravenous potassium chloride. Demographic and laboratory data on children receiving intravenous potassium chloride in the pediatric intensive care unit and details of the drug order were analyzed. MEASUREMENTS AND MAIN RESULTS: Data from 1,492 intravenous potassium chloride administration-events before implementation of the drug request form were collected. After the drug request form was mandated, 166 consecutively completed forms were collected and analyzed. The incidence of postinfusion elevations in serum potassium decreased from a rate of 7.7% (103 of 1,341) before the drug request form to 0% (0 of 150) after the drug request form (p < .001). Proximal causes of error were also reduced. The number of patients with a creatinine >/=2 mg/dL receiving intravenous potassium chloride decreased from 28.4% to 14.2% (p < .001). The number of intravenous potassium chloride infusions administered to patients where serum potassium value was >4.5 mmol/L decreased significantly (2.9% vs. 0.0%, p < .02). The incidence rates of both verbal orders and failure to write the order in a correct format were reduced to zero. CONCLUSIONS: Simple, blame-free, system-wide interventions designed to reduce proximal causes of error can be an effective, proactive means of reducing the likelihood of medical morbidity.

Adolescent↗

Diffusion in immobilized-cell agar layers: influence of bacterial growth on the diffusivity of potassium chloride.

The diffusivity of potassium chloride in composite agar slab/microporous membrane structures loaded with various amounts of Escherichia coli whole cells was determined using both time-lag and steady-state methods. The diffusion coefficient of KCl decreased linearly with the logarithm of the immobilized-cell content. The effect exerted by bacterial growth inside the immobilization matrices on KCl diffusivity was then investigated. The diffusion coefficient of KCl obtained by time-lag analysis decreased during incubation of the immobilized-cell structures, whereas less consistent results arose from the steady-state method. An apparent doubling time for immobilized E. coli, increasing with the initial cell content of the gel, was obtained from the calibration relationship between KCl diffusivity and the number of organisms in agar.

Culture Media↗

Pharmacokinetics and effects on fecal blood loss of a controlled release potassium chloride tablet.

A slow-release tablet containing 12.5 mEq of potassium chloride was compared with a potassium chloride solution in normal human subjects under controlled conditions. Changes in plasma potassium concentration and rates of urinary potassium excretion indicate the tablet is absorbed in a slow, sustained fashion in contrast to the solution. Net potassium excretion after single and multiple doses indicates that the amount of potassium absorbed from the slow-release tablet is comparable to the solution. The slow-release potassium chloride tablets were well tolerated and were effective in correcting experimentally induced potassium depletion of moderate severity. Gastrointestinal tract irritation was not apparent and fecal 51Cr red blood cell loss after the tablet and the solution were of the same order.

Adolescent↗

Effectiveness of potassium chloride or triamterene in thiazide hypokalemia.

Potassium chloride was compared with triamterene in a crossover trial involving 16 hypertensive patients with overt diuretic-induced hypokalemia. Potassium chloride, 24 to 96 mEq/day, normalized the plasma potassium (PK) level at 3.5 mEq/L or more in only eight of the patients. The average increase in PK level was 0.58 mEq/L. Triamterene, 50 to 200 mg daily, normalized PK level in ten of the patients. The average increase in PK level was 0.72 mEq/L, which was not significantly different than that with potassium therapy. Some patients who responded to potassium did not respond to triamterene, and vice versa. Most of the administered potassium was excreted in the urine even with persisting hypokalemia. Addition of triamterene to diuretic therapy resulted in a small but statistically significant increase in plasma creatinine level.

Adult↗

Potassium-magnesium citrate versus potassium chloride in thiazide-induced hypokalemia.

BACKGROUND: The purpose of this study was to compare the value of potassium-magnesium citrate (KMgCit) with potassium chloride in overcoming thiazide-induced hypokalemia. METHODS: Sixty normal subjects first took hydrochlorothiazide (HCTZ; 50 mg/day). After three weeks of treatment (or earlier if hypokalemia developed), they were randomized to take KMgCit (42 mEq K, 21 mEq Mg, and 63 mEq citrate/day) or potassium chloride (42 mEq/day) for three weeks while continuing on HCTZ. RESULTS: KMgCit significantly increased the serum potassium concentration from 3.42 +/- 0.30 mEq/L on HCTZ alone to about 3.8 mEq/L (P < 0.001). Potassium chloride produced a similar increase in serum potassium concentration from 3.45 +/- 0.44 mEq/L to about 3.8 mEq/L (P < 0. 001). KMgCit significantly increased the serum magnesium concentration by 0.11 to 0.12 mEq/L (P < 0.01), whereas potassium chloride produced a marginal decline or no significant change. KMgCit was less effective than potassium chloride in correcting HCTZ-induced hypochloridemia and hyperbicarbonatemia. KMgCit, but not potassium chloride, significantly increased urinary pH (by about 0.6 unit), citrate (by about 260 mg/day), and urinary magnesium. CONCLUSIONS: KMgCit is equally effective as potassium chloride in correcting thiazide-induced hypokalemia. In addition, KMgCit, but not potassium chloride, produces a small but significant increase in serum magnesium concentration by delivering a magnesium load, and it confers alkalinizing and citraturic actions.

Adult↗

Increased potassium, chloride, and taurine conductances in astrocytes during hypoosmotic swelling.

Membrane conductances during hypoosmotic swelling were characterized in rat astrocytes in primary tissue culture. Using whole cell patch clamp techniques, mean +/- SEM cell conductance in isoosmotic phosphate-buffered saline (PBS) was 55.6 +/- 5.8 pS/pF. Cell conductance (mean +/- SEM) increased from this initial value to 187 +/- 46%, 561 +/- 188%, and 1216 +/- 376% within 9 min of exposure to 220 mOsm, 190 mOsm, and 145 mOsm PBS, respectively. With each of these hypoosmotic exposures, no change occurred in membrane capacitance. When CsCl replaced KCl in the microelectrode solution, a similar conductance increase was obtained at each osmolality. However, when gluconate salts were used in place of chloride salts in the electrode solution, no significant conductance increase was observed with 190 mOsm PBS. With a KCl microelectrode solution, all conductance increase which occurred in 190 mOsm PBS was inhibited by 200 microM niflumic acid, but not by 5 mM BaCl(2). Both niflumic acid and BaCl(2) inhibited 60-80% of the conductance increase of cells in 145 mOsm PBS. Using a microelectrode solution containing taurine as the major anion, membrane conductance increased 5-fold when cells were placed in 250 mOsm medium. This conductance increase was completely inhibited by 200 microM niflumic acid. Thus, independent chloride and potassium conductances are activated by hypoosmotic swelling of cultured astrocytes while plasma membrane area is unaltered. The chloride conductance pathway is activated at a significantly lower degree of hypoosmotic exposure than that which activates the potassium pathway and may be permeable to anionic taurine. These conductance pathways may mediate diffusive loss of potassium, chloride, and taurine from these cells during volume regulation following hypoosmotic swelling.

Animals↗

The influence of oral potassium chloride on blood pressure in hypertensive men on a low-sodium diet.

Clinical and epidemiologic studies suggest that the intake of potassium chloride lowers blood pressure. To investigate whether supplemental potassium chloride (96 mmol of microcrystalline potassium chloride a day) reduced the need for antihypertensive medication in hypertensive men on a restricted-sodium diet, we conducted a randomized, placebo-controlled, double-blind clinical trial. A total of 287 men 45 to 68 years of age, 142 given potassium chloride and 145 given placebo, were followed for an average of 2.2 years after the withdrawal of their antihypertensive medication. Men in both groups received instructions on following a low-sodium diet. Overnight urinary sodium excretion fell from 63 mmol per eight hours at base line to an average of 45 mmol per eight hours during follow-up. Participants given supplemental potassium chloride had significantly higher (P less than 0.001) serum potassium levels and urinary potassium excretion (averaging 4.5 mmol per liter and 42.5 mmol per eight hours, respectively) during follow-up than participants given placebo (4.2 mmol per liter and 20.0 mmol per eight hours). Seventy-nine participants in each group required reinstitution of antihypertensive medication according to strict indications defined by the protocol. No significant differences in systolic or diastolic blood pressure were observed between the two groups. During follow-up, systolic and diastolic blood pressure averaged 130.6 and 82.5 mm Hg, respectively, for participants given supplemental potassium, and 132.5 and 83.1 mm Hg for participants given placebo. We conclude that supplemental potassium chloride does not reduce the need for antihypertensive medication in hypertensive men on a restricted-sodium diet.

Administration, Oral↗

What is the better formulation of microencapsulated potassium chloride?

A single blind cross-over study was performed comparing a new microencapsulated potassium chloride tablet (MET) with two reference formulations of oral potassium, namely potassium chloride solution (PS), and microencapsulated potassium chloride capsules (MEC), in 18 normal healthy volunteers. The potassium chloride induced change in gastric potential difference (PD) of the mucosa was the main criterion of comparison and was assessed by the area above curve (AAC), the total duration of the effect (TDE), the maximal variation of PD (delta MAX), and the aggression index (AI). The results showed that all three formulations induced a fall in PD; the delta MAX and AAC were significantly greater for PS indicating a higher aggressive effect of the solution; MET had significantly less aggressive effect than MEC when assessed by all parameters.

Adult↗

Renal potassium-chloride cotransporters.

The electroneutral cotransport of potassium and chloride is mediated by potassium-chloride transporters, which are encoded by members of the gene family of cation-chloride cotransporters. A significant body of evidence argues for swelling-activated, basolateral potassium-chloride transport in the proximal tubule and thick ascending limb, with a potential role in transepithelial salt transport. However, the lack of specific inhibitors has impeded progress in this area. The cloning of the four potassium-chloride cotransporter genes has sparked new interest in this transport pathway, and promises to yield novel insights into their roles in cellular and renal physiology.

Amino Acid Sequence↗

Adequacy of twice daily dosing with potassium chloride and spironolactone in thiazide treated hypertensive patients.

1. The effects of 4-6 weeks treatment with placebo, potassium chloride 32 mmol 12 hourly, and spironolactone 25 mg 12 hourly upon the plasma potassium concentration-time profile were examined in hypertensive patients taking bendrofluazide 5 mg daily. 2. When compared with placebo, potassium chloride increased peak plasma potassium concentration (P less than 0.05), 12 h AUC for plasma potassium (P less than 0.1), and 12 h urine potassium excretion (P = 0.002). Spironolactone increased peak plasma potassium concentration (P less than 0.05), and 12 h AUC for plasma potassium (P less than 0.05), compared with placebo values. 3. Potassium chloride and spironolactone did not differ significantly in any respect other than 12 h urine potassium excretion. The 12 h AUC for plasma potassium was 35% larger with spironolactone than potassium chloride (not significant). 4. With both active drugs peak plasma potassium was observed 2-3 h after dosing, and efficacy tended to wane towards 12 h. However, variability of plasma potassium within the dose interval was not increased markedly, and 12 hourly dosing is probably satisfactory for both potassium chloride and spironolactone at the doses studied.

Adult↗

Rapid correction of hypokalemia using concentrated intravenous potassium chloride infusions.

There are conflicting recommendations regarding the use of intravenous potassium chloride infusions for acute correction of hypokalemia. We examined the effects of 495 sets of potassium chloride infusions administered to a medical intensive care unit population. The infusion sets consisted of one to eight consecutive individual infusions, each containing 20 mEq of potassium chloride in 100 mL of saline administered. The mean preinfusion potassium level was 3.2 mmol/L, and the mean postinfusion potassium level was 3.9 mmol/L. The mean increment in serum potassium level per 20-mEq infusion was 0.25 mmol/L. No temporally related life-threatening arrhythmias were noted; however, there were 10 instances of mild hyperkalemia. Our data endorse the relative safety of using concentrated (200-mEq/L) potassium chloride infusions at a rate of 20 mEq/h via central or peripheral vein to correct hypokalemia in patients in the intensive care unit.

Catheterization, Central Venous↗

[Inhibition of growth of E. coli cells by anolites of sodium and potassium chloride after processing solutions in a diaphragmatic electrolyzer].

The relationship between the inhibitory effect of sodium chloride and potassium anolites, obtained in a diaphragm electrolyser, and the physicochemical parameters of solutions was compared with that between the inhibitory effect and physicochemical properties of hypochlorites obtained after treating the solutions in an electrolyser having no diaphragm was compared. The biological activity of solutions containing molecular chlorine, hypochlorous acid, and hypochlorite ions was determined by their effect on the growth of E. coli cells. After a 5-min incubation of cells with each of the oxidizers, the bacterial growth stopped and was not restored during one day. The conclusion is made that the oxidizers irreversibly disturb the barrier properties of cell membranes and, in some cases, destroy cells. In model solutions, as well as in solutions treated after heating on a water bath or after the addition of sodium thiosulfate, a delay in the start of E. coli growth occurs. After the lag-phase, the repair of cells sets on, and after a day the optical density of cells increases and approaches the control.

Electrochemistry↗