Sodium concentrations

Some additional methods of classification are under development that center on the use of lignite for combustion in utihty boilers or electric power generation. Correlations based on the sodium concentration in the lignitic ash (10), or soluble A1 concentration (11) are used. The classifications are often given in terms of the severity of boiler fouling. 

Iron, cobalt, and nickel catalyze this reaction. The rate depends on temperature and sodium concentration. At —33.5°C, 0.251 kg sodium is soluble in 1 kg ammonia. Concentrated solutions of sodium in ammonia separate into two Hquid phases when cooled below the consolute temperature of —41.6°C. The compositions of the phases depend on the temperature. At the peak of the conjugate solutions curve, the composition is 4.15 atom % sodium. The density decreases with increasing concentration of sodium. Thus, in the two-phase region the dilute bottom phase, low in sodium concentration, has a deep-blue color the light top phase, high in sodium concentration, has a metallic bronze appearance (9—13). 

In the inner ear, ENaC is expressed in supporting cells surrounding hair cells and is postulated to play a role in the low sodium concentration of endolymph, critical for proper mechanotransduction and hearing. 

Acute over-activation of NHE1 results in a marked elevation in intracellular sodium concentration with a subsequent increase in intracellular calcium, via the Na +/Ca++ exchanger. This in turn triggers a cascade of injurious events that can culminate in tissue dysfunction and ultimately apoptosis and necrosis. This is commonly seen in organs such as the heart, brain and kidneys as a consequence of ischemia-reperfusion. 

Neurotransmitter transport can be electrogenic if it results in the net translocation of electrical charge (e.g. if more cations than anions are transferred into the cell interior). Moreover, some transporters may direction-ally conduct ions in a manner akin to ligand-gated ion channels this ion flux is not coupled to substrate transport and requires a separate permeation pathway associated with the transporter molecule. In the case of the monoamine transporters (DAT, NET, SERT) the sodium current triggered by amphetamine, a monoamine and psychostimulant (see Fig. 4) is considered responsible for a high internal sodium concentration... 

Na Influx Studies. Na influx was monitored according to the procedure of Owen and Villereal (34), with some modifications. Cells were seeded onto 60-mm culture dishes, grown, and serum starved as described for the assays above. The cells were washed with incubation media and incubated in 3 ml of the appropriate agent at 37 C. After incubation the cells were rapidly washed in ice cold 0.1 mM MgCL and extracted with 5% TCA/0.5% KNO3 for sodium determination or 0.2% SDS for protein determination. Sodium concentration was measured using a Varian Model 275 Atomic Absorption Spectrophotometer. Protein was determined fluorimetrically. 

Assuming that the initial sodium concentration of glass particle with a radius R is C, and its surface sodium concentration Cj is zero at t > 0, dimensionless terms can be written as... 

Table 8 5 shows that each of the four common s-block ions is abundant not only in seawater but also in body fluids, where these ions play essential biochemical roles. Sodium is the most abundant cation in fluids that are outside of cells, and proper functioning of body cells requires that sodium concentrations be maintained within a narrow range. One of the main functions of the kidneys is to control the excretion of sodium. Whereas sodium cations are abundant in the fluids outside of cells, potassium cations are the most abundant ions in the fluids inside cells. The difference in ion concentration across cell walls is responsible for the generation of nerve impulses that drive muscle contraction. If the difference in potassium ion concentration across cell walls deteriorates, muscular activity, including the regular muscle contractions of the heart, can be seriously disrupted. 

Serum sodium may rise with insulin and isotonic saline fluid administration. Estimate the corrected serum sodium concentration at presentation... 

When plasma glucose falls to <250 mg/dL, switch to D5W, D5W/half NS, or D5W/NS depending on plasma sodium concentration... 

Estimate the corrected serum sodium concentration at presentation... 

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... 

While some clinical and laboratory findings assist in the general diagnosis of ARF, others are used to differentiate between prerenal, intrinsic, and postrenal ARF. For example, patients with prerenal ARF typically demonstrate enhanced sodium reabsorption, which is reflected by a low urine sodium concentration and a low fractional excretion of sodium. Urine is typically more concentrated with prerenal ARF and there is a higher urine osmolality and urine plasma creatinine ratio compared to intrinsic and postrenal ARF. 

Describe the unique relationship between serum sodium concentration and total body water. 

The tonicity of crystalloid solutions is directly related to their sodium concentration. The most commonly used crystalloids include normal saline, hypertonic saline, and lactated Ringer s solution. Excessive administration of any fluid replacement therapy, regardless of tonicity, can lead to fluid overload, particularly in patients with cardiac or renal insufficiency. 

Half-normal saline is a hypotonic fluid that provides free water in relative excess when compared to the sodium concentration. This crystalloid is typically used to treat patients... 

The body s normal daily sodium requirement is 1.0 to 1.5 mEq/kg (80 to 130 mEq, which is 80 to 130 mmol) to maintain a normal serum sodium concentration of 136 to 145 mEq/L (136 to 145 mmol/L).15 Sodium is the predominant cation of the ECF and largely determines ECF volume. Sodium is also the primary factor in establishing the osmotic pressure relationship between the ICF and ECF. All body fluids are in osmotic equilibrium and changes in serum sodium concentration are associated with shifts of water into and out of body fluid compartments. When sodium is added to the intravascular fluid compartment, fluid is pulled intravascularly from the interstitial fluid and the ICF until osmotic balance is restored. As such, a patient s measured sodium level should not be viewed as an index of sodium need because this parameter reflects the balance between total body sodium content and TBW. Disturbances in the sodium level most often represent disturbances of TBW. Sodium imbalances cannot be properly assessed without first assessing the body fluid status. 

Hyponatremia is very common in hospitalized patients and is defined as a serum sodium concentration below 136 mEq/L (136 mmol/L). Clinical signs and symptoms appear at concentrations below 120 mEq/L (120 mmol/L) and typically consist of agitation, fatigue, headache, muscle cramps, and nausea. With profound hyponatremia (less than 110 mEq/L [110 mmol/L]), confusion, seizures, and coma maybe seen. Because therapy is also influenced by volume status, hyponatremia is further defined as (1) hypertonic hyponatremia (2) hypotonic hyponatremia with an increased ECF volume (3) hypotonic hyponatremia with a normal ECF volume and (4) hypotonic hyponatremia with a decreased ECF volume.16... 

Although both water and sodium are required in this instance, sodium needs to be provided in excess of water to fully correct this abnormality. As such, hypertonic saline (3% NaCl) is often used. One can estimate the change in serum sodium concentration after 1 L of 3% NaCl infusion using the following equation 16... 

Estimate the anticipated change in serum sodium concentrations after the infusion of 1 L of 3% sodium chloride in a 75-kg male with a serum sodium of 123 mEq/L (123 mmol/L). 

Hypernatremia is a serum sodium concentration greater than 145 mEq/L (145 mmol/L) and can occur in the absence of a sodium deficit (pure water loss) or in its presence (hypotonic fluid loss).19 The signs and symptoms of hypernatremia are the same as those found in TBW depletion. Symptoms of hypernatremia are evident with a serum concentration greater than 160 mEq/L (160 mmol/L) and usually consist of thirst, mental slowing, and dry mucous membranes. Signs and symptoms become more profound as hypernatremia worsens, with the patient demonstrating confusion, hallucinations, acute weight... 

What is the likely cause for the increased sodium concentration in this patient ... 

Now consider a psychiatric patient who presents with a pH of 7.50, a PaC02 of 20 mm Hg (2.7 kFh), an HC03 of 16 mEq/L (mmol/L), a sodium concentration of 140 mEq/L (mmol/L), and a chloride level of 103 mEq/L (mmol/L). Because this person is alkalemic, the low PaC02 is the primary disturbance and represents respiratory alkalosis. If this disturbance is a chronic respiratory alkalosis with metabolic compensation, the expected AHC03 is 0.4 x APaC02 (in millimeters of mercury) or 0.4 x 20, which is 8 mEq/L (mmol/L). As such, the predicted HC03 concentration should be 24 mEq/L (mmol/L) [normal] - 8 mEq/L (mmol/L) [expected compensation] or 16 mEq/L (16 mmol/L). 

Oxcarbazepine Hyponatremia (serum sodium concentrations less than 125 mEq/L) has been reported and occurs more frequently during the first 3 months of therapy serum sodium concentrations should be monitored in patients receiving drugs that lower serum sodium concentrations (e.g., diuretics or drugs that cause inappropriate antidiuretic hormone secretion) or in patients with symptoms of hyponatremia (e.g., confusion, headache, lethargy, and malaise). Hypersensitivity reactions have occurred in approximately 25-30% of patients with a history of carbamazepine hypersensitivity and requires immediate discontinuation. 

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