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Topic: Hypobicarbonatemia


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  Hypobicarbonatemia Encyclopedia Article, History, Biography at Karr.net   (Site not responding. Last check: 2007-11-04)
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www.karr.net /encyclopedia/Hypobicarbonatemia   (134 words)

  
 Patil81, Chapter 3
Because the concentration of K and HCO3 in the lower GI fluid is greater than in the plasma, there is also a corresponding reduction in the serum concentration of K (called hypokalemia) and HCO3 (called hypobicarbonatemia) in the extracellular fluid.
Finally, because the concentration of Cl and Na in the lower GI fluid is lower than that in the plasma, there is corresponding increase in the concentration of Cl (called hyperchloremia) and Na (called hypernatremia) in the extracellular fluid.
Hypobicarbonatemia is interpreted as metabolic acidosis at the next higher level of detail.
www.medg.lcs.mit.edu /people/psz/PatilThesis81/Patil81_ch3.html   (4239 words)

  
 In certain organic acidoses (e   (Site not responding. Last check: 2007-11-04)
If substantial component of hyperchloremic acidosis (relatively normal anion gap) due to urinary loss of ketoacid anions- can benefit from alkali therapy, even when acidemia is moderately severe.
Loss of bicarbonate from the digestive tract can lead to marked metabolic acidosis that requires exogenous replenishment of body alkali stores, in addition to replenishment of water, sodium, and potassium.
Endogenous correction of the hypobicarbonatemia depends largely on increased renal acid excretion, -  requiring several days.
www.mindwheels.com /ED-WEB%20Web/Acid_base.htm   (598 words)

  
 Indian Pediatrics - Editorial
In general, the lower the pretreatment HCO3–, more the bicarbo-nate that is needed to produce a given increase in HCO3–.
In patients with mild or moderate hypobicarbonatemia, about ¼ to ½ of infused bicarbonate remains unneutralized in the ECF.
Thus, if 60 mmol bicarbonate is infused, 15-30mmol will remain, and ECF HCO3– will rise by about 1-2 mmol/L. In severe hypobicarbo-natemia, only 1/8 to 1/4 of infused bicarbonate remains unneutralized in the ECF.
www.indianpediatrics.net /may2002/may-508-509.htm   (792 words)

  
 Modeling Knowledge of the Patient in Acid-Base and Electrolyte Disorders
Therefore, lower GI losses occurring without proper replacement of electrolytes and water will result in hypobicarbonatemia, hypokalemia, hyperchloremia, hypernatremia, and volume-loss, as shown in Fig.
The metabolic acidosis along with moderate hypocapnia causes hypobicarbonatemia.
The hypobicarbonatemia along with hypocapnia causes mild acidemia.
medg.lcs.mit.edu /ftp/psz/AIM82/ch6.html   (13100 words)

  
 Patil81, Chapter 2   (Site not responding. Last check: 2007-11-04)
The chronic respiratory alkalosis and acute respiratory acidosis along with mild acidemia cause moderate hypocapnia, which causes hypobicarbonatemia.
The cycles present at the intermediate level describing the interaction between the acidemia, hypobicarbonatemia and hypocapnia have been abstracted away.
In the first case, the change in the acid-base state is a consequence of loss of HCQ3 from the body which causes hypobicarbonatemia, whereas in the second it enters as primary disturbance in ventilation which alters the PCO2.
medg.lcs.mit.edu /people/psz/PatilThesis81/Patil81_ch2.html   (2848 words)

  
 METABOLIC ACIDOSIS
Metabolic acidosis is an abnormally low bicarbonate level (<18 mEq/L) and a pH <7.35.
With the exception of renal compensation for respiratory alkalosis, hypobicarbonatemia is abnormal.
Again, if you think about it, non-compensated hypobicarbonatemia is metabolic acidosis.
www.capefearvalley.com /outreach/outreach/modules/AcidBase/Pages/MetabolicAcidosis.htm   (437 words)

  
 Patil81, Chapter 6
In the first case, the change in acid-base state is a consequence of addition of H
to the body which causes hypobicarbonatemia, whereas in the second it enters as primary disturbance in ventilation which alters the CO2 tension.
The pathophysiological level differences between the two cases can be identified similarly by comparing the two pathophysiological level descriptions.
www.cdm.csail.mit.edu /ftp/patil/PatilThesis81/Patil81_ch6.html   (3259 words)

  
 Cecil Textbook of Medicine : />
Readily measured blood and urine chemistries may offer some clues to diagnosis.
In theory, PTH hypersecretion should be reflected by hypophosphatemia, hyperchloremia, hypobicarbonatemia, increased urinary phosphate excretion, and urinary calcium excretion that is relatively low for the filtered load.
PTH secretion suppressed by hypercalcemia of nonparathyroid etiology should, in theory, reverse these parameters.
www.merckmedicus.com /ppdocs/us/common/cecils/chapters/260_008.htm   (560 words)

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