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Serum bicarbonate

During therapy, the nurse periodically obtains (daily or more frequently) serum electrolyte or bicarbonate studies to monitor therapy. [Pg.642]

Treatment depends on degree of hyperkalemia and presence/severity of signs and symptoms (sometimes irrespective of actual serum potassium level). Mild 5.5-6 mEq/L—furosemide and sodium polystyrene sulfonate. Moderate 6.1-7 mEq/L—insulin, glucose, sodium bicarbonate,... [Pg.166]

Low serum chloride and elevated serum bicarbonate levels indicate metabolic alkalosis. [Pg.297]

Patients with acute hyperkalemia usually require other therapies to manage hyperkalemia until dialysis can be initiated. Patients who present with cardiac abnormalities caused by hyperkalemia should receive calcium gluconate or chloride (1 g intravenously) to reverse the cardiac effects. Temporary measures can be employed to shift extracellular potassium into the intracellular compartment to stabilize cellular membrane effects of excessive serum potassium levels. Such measures include the use of regular insulin (5 to 10 units intravenously) and dextrose (5% to 50% intravenously), or nebulized albuterol (10 to 20 mg). Sodium bicarbonate should not be used to shift extracellular potassium intracellularly in patients with CKD unless severe metabolic acidosis (pH less than 7.2) is present. These measures will decrease serum potassium levels within 30 to 60 minutes after treatment, but potassium must still be removed from the body. Shifting potassium to the intracellular compartment, however, decreases potassium removal by dialysis. Often, multiple dialysis sessions are required to remove potassium that is redistributed from the intracellular space back into the serum. [Pg.382]

Studies have demonstrated that reversal of metabolic acidosis can improve bone disease associated with CKD.38 Serum bicarbonate levels should be maintained at 22 mEq/L (22 mmol/L) in patients with bone disease associated with CKD.39 The treatment of metabolic acidosis is described below. [Pg.391]

As kidney function declines, bicarbonate reabsorption is maintained, but hydrogen excretion is decreased because the ability of the kidney to generate ammonia is impaired. The positive hydrogen balance leads to metabolic acidosis, which is characterized by a serum bicarbonate level of 15 to 20 mEq/L (15 to 20 mmol/L). This picture is generally seen when the GFR declines below 20 to 30 mL/minute.38... [Pg.392]

Pharmacologic therapy with sodium bicarbonate or citrate/citric acid preparations maybe needed in patients with stage 3 CKD or higher to replenish body stores of bicarbonate. Calcium carbonate and calcium acetate, used to bind phosphorus in sHPT, also aid in increasing serum bicarbonate levels, in conjunction with other agents. [Pg.392]

When determining the dose of bicarbonate replacement, the goal for therapy is to achieve a normal serum bicarbonate level of 24 mEq/L (24 mmol/L). The dose is usually determined by calculating the base deficit [0.5 L/kg X (body weight)] x [(normal C02) - (measured C02)]. Because of the risk of volume overload resulting from the sodium load administered with bicarbonate replacement, the total base deficit should be administered over several days. Once the goal serum bicarbonate level is attained, a maintenance dose of bicarbonate is necessary and should be titrated to maintain serum bicarbonate levels. [Pg.392]

The extracellular fluid (ECF) is the fluid outside the cell and is rich in sodium, chloride, and bicarbonate. O The ECF is approximately one-third of TBW (14 L in a 70-kg man or 12 Lin a 70-kg woman) and is subdivided into two compartments the interstitial fluid and the intravascular fluid. The interstitial fluid (also known as lymphatic fluid) represents the fluid occupying the spaces between cells, and is about 25% of TBW (10.5 L in a 70-kg man or 8.8 L in a 70-kg woman). The intravascular fluid (also known as plasma) represents the fluid within the blood vessels and is about 8% of TBW (3.4 L in a 70-kg man or 2.8 L in a 70-kg woman). The ECF is approximately one-third of TBW or 14 L in a 70-kg male. Because the exact percentages are cumbersome to recall, many clinicians accept that the ECF represents roughly 20% of body weight (regardless of gender) with 15% in the interstitial space and 5% in the intravascular space.6 Note that serum electrolytes are routinely measured from the ECF. [Pg.404]

Normally, the number of anions and cations in each fluid compartment are equal. Cell membranes play the critical role of maintaining distinct ICF and ECF spaces which are biochemically distinct. Serum electrolyte concentrations reflect the stores of ECF electrolytes rather than that of ICF electrolytes. Table 24-4 lists the chief cations and anions along with their normal concentrations in the ECF and ICF. The principal cations are sodium, potassium, calcium, and magnesium, while the key anions are chloride, bicarbonate, and phosphate. In the ECF, sodium is the most common cation and chloride is the most abundant anion while in the ICF, potassium is the primary cation and phosphate is the main anion. Normal serum electrolyte values are listed in Table 24—5. [Pg.407]

Because C02 is a volatile acid, it can rapidly be changed by the respiratory system. If a respiratory acid-base disturbance is present for minutes to hours it is considered an acute disorder while if it is present for days or longer it is considered a chronic disorder. By definition, the metabolic machinery that regulates HC03 results in slow changes in serum bicarbonate and all metabolic disorders are chronic. This means that there are six simple acid-base disorders as outlined in Table 25-1.2... [Pg.421]

It is important to realize that the serum HCO, concentration may be affected by the presence of unmeasured endogenous acids (lactic acidosis or ketoacidosis). Bicarbonate will attempt to buffer these acids, resulting in a 1 mEq loss of serum HCO, for each 1 mEq of acid titrated. Because the cation side of the equation is not affected by this transaction, the loss of serum HC03 results in an increase in the calculated anion gap. Identification of an increased anion gap is very important for identifying the etiology of the acid-base disorder. The concept of the increased anion gap will be applied later in the case studies section. [Pg.424]

None unless symptoms present => Consider lactate concentrations in patients with 4- serum bicarbonate or T anion gap... [Pg.1269]

Etoposide Blood pressure, respiratory rate, serum pH, serum bicarbonate with arterial blood gases, and evaluation of anion gap if necessary... [Pg.1464]

Vigorous intravenous hydration with dextrose 5% in water with half-normal saline at 3 L/m2 per day to maintain a urine output of 100 mL/m2 per hour or more is necessary, unless the patient presents with acute renal dysfunction. Alkalinization of the urine to a pH of 7.0 or more with 50 to 100 mEq/L of sodium bicarbonate has been used to promote uric acid solubility for excretion. This measure is controversial because xanthine and hypoxanthine are less soluble at alkaline pH, potentially leading to crystallization, especially during and after allopurinol therapy32 (see Fig. 96-6). Medications that increase serum... [Pg.1487]

Electrolytes Daily doses based on daily maintenance requirements, renal function, gastrointestinal losses, acid-base status, concomitant drug therapy, nutritional and anabolic status Pa lion I has hyponatremia, hypokalemia, hypomagnesemia, and hypophosphatemia, also has low serum bicarbonate concentration, could be component of metabolic acidosis due to sepsis... [Pg.1503]

FIGURE 5.8 Complex hyperfine patterns due to axes noncolinearity in a low-symmetry prosthetic group. The X-band spectrum is from 65Cu(II)-bicarbonate in human serum transferrin (a,b) experimental spectrum (c,e) simulation assuming axial symmetry (d, f) simulation assuming triclinic symmetry with the A-axes rotated with respect to the g-axes over 15° about the gz-axis and then 60° about the new y -axis. Traces b, e, and f are 5x blow-ups of traces a, c, d, respectively (Hagen 2006). (Reproduced by permisson of The Royal Society of Chemistry.)... [Pg.81]

The kidney exerts control over the concentration of bicarbonate. The initial filtrate of the kidney has the same buffer composition (except for the proteins) as serum. Based on the pH of the initial filtrate, the kidney can decide to reclaim the initially filtered bicarbonate and place it back in the serum, or it can decide to just let it go out of the body. If the kidney does not reclaim bicarbonate, the serum bicarbonate concentration falls. If the kidney reclaims more bicarbonate than normal, the bicarbonate concentration rises. [Pg.270]

Normally, everything is balanced, C02 and bicarbonate are removed at exactly the same rate that they re formed, and the pH of the serum remains very close to 7.4. If for some reason the lungs blow off too much C02 by hyperventilating (breathing too fast), the numerator of the magic equation (pC02) decreases, and, as long as [HCO 3] remains constant, the [H+] must decrease (pH increases). [Pg.270]

Current nutritional intake Complete blood cell count Serum electrolytes Sodium Potassium Chloride Bicarbonate Magnesium Phosphorous Calcium Serum glucose Serum albumin Markers for organ function Liver function tests Alkaline phosphatase Aspartate aminotransferase Alanine aminotransferase Total bilirubin Prothrombin time or International normalized ratio Renal function tests Blood urea nitrogen Creatinine Fluid balance Input Oral... [Pg.690]

Serum electrolytes Sodium Potassium Chloride Bicarbonate Magnesium Phosphorous Calcium... [Pg.690]

Sodium potassium chloride, bicarbonate calcium phosphate, magnesium Blood urea nitrogen/serum creatinine Drugs and their dosing regimens Nutritional regimen Blood glucose... [Pg.869]

The replacement alkali dose can be approximated by multiplying bicarbonate s volume of distribution (0.5 L/kg) by the patient s weight (in kg) and by their deficit (24 mEq/L minus patient s serum bicarbonate value). The dose should be administered over several days. The daily maintenance dose is usually 12 to 20 mEq/mL and should be titrated as needed. [Pg.886]

In a study with human subjects, whose urine pH was controlled with sodium bicarbonate and ammonium chloride, it was found that 10-25% of the administered pseudoephedrine hydrochloride was metabolized to norpseudoephedrine and the elimination of pseudoephedrine and norpseudoephedrine was related to urine pH. As the urine pH increased, the serum half-life of pseudoephedrine and norpseudoephedrine increased.15 In another similar study it was found that a decrease... [Pg.497]

Hyperchloremic acidosis has been noted in some cases (B7, K13) this is presumably due to defective tubular reabsorption of bicarbonate. Phosphate-losing rickets or marked hypokalemia have not as yet been reported in galactosemia, but some cases show roentgenological evidence of osteoporosis (M2), and Holzel et al. (H8) record low levels of serum potassium. [Pg.21]

Seek T75 plastic tissue culture flasks with a minimum of 2.5 x 106 cells in 120ml of Eagle s medium containing 20mM L-glutamine 0.88g l-1 sodium bicarbonate 20 mM HEPES 50 pg ml-1 streptomycin sulphate 50IUml 1 benzyl-penicillin and 7.5% fetal bovine serum. The flasks are incubated for 18-24 h at 37°C in a C02 incubator to establish monolayer cultures. [Pg.207]


See other pages where Serum bicarbonate is mentioned: [Pg.28]    [Pg.138]    [Pg.11]    [Pg.88]    [Pg.288]    [Pg.411]    [Pg.412]    [Pg.419]    [Pg.424]    [Pg.424]    [Pg.425]    [Pg.426]    [Pg.662]    [Pg.662]    [Pg.663]    [Pg.691]    [Pg.1489]    [Pg.116]    [Pg.271]    [Pg.883]   
See also in sourсe #XX -- [ Pg.420 , Pg.421 , Pg.422 , Pg.423 ]

See also in sourсe #XX -- [ Pg.47 ]




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