Plasma bicarbonate

Any body tissue in direct equilibrium with the major excretum should reflect the isotopic composition of the diet as a whole. This seems to be the case for bioapatite carbonate, which is thought to be in equilibrium with plasma bicarbonate, which itself is in equilibrium with respired CO2. In fact the Ambrose and Norr (1993) and Tieszen and Fagre (1993) data sets (among others) show clearly that the bioapatite carbonate differs from total diet (or respired CO ) by an amount approximating to the equilibrium isotopic fractionation in the system (Mook 1989) ... 

Metabolic acidosis is characterized by decreased plasma bicarbonate concentrations (HC03 ), whereas metabolic alkalosis is characterized by increased HC03T... 

In metabolic alkalosis and respiratory acidosis, pH does not usually deviate significantly from normal, but treatment can be required to maintain Pao2 and PaC02 at acceptable levels. Treatment should be aimed at decreasing plasma bicarbonate with sodium and potassium chloride therapy, allowing renal excretion of retained bicarbonate from diuretic-induced metabolic alkalosis. 

Bicarbonate ions secreted into the blood stream help maintain the normal plasma bicarbonate concentration of approximately 25 mmol/1, whilst the two protons are secreted into the lumen of the proximal tubule in exchange for sodium via a Na+/H+ antiport. 

Pharmacology Increases plasma bicarbonate buffers excess hydrogen ion concentration raises blood pH reverses the clinical manifestations of acidosis. 

The clinical biochemical features reflect the biochemical and physiological effects. Thus, there is reduced plasma bicarbonate, low plasma calcium, and raised potassium. Crystals, blood, and protein may all be detected in the urine (crystalluria, hematuria, and proteinuria, respectively), and the urine may have a low specific gravity. 

There is a good deal of support for such an origin of the carbonate ion. Certainly, in invertebrates there are conclusive kinetic data based on radioisotope studies to show that, although the blood supplies Ca2+ for egg shell formation, the plasma bicarbonate plays no direct role602). 

Six experts in intensive care or metabolic disease reviewed all case reports of lactic acidosis from 1957 to 1999—37 articles reporting 80 cases (85). To be assessed the reports had to meet strict criteria, including a diagnosis of type 2 diabetes, metformin therapy before lactic acidosis, a pH of 7.35 or less, or a plasma bicarbonate concentration below 22 mmol/1 and a lactic acid concentration of at least 5 mmol/1. Because of lack of information, 33 cases were excluded. There were other susceptibility factors for lactic acidosis besides metformin in 46 of 47 cases. Only 13 of the 47 cases were classified as probably due to metformin by at least three experts. The authors suggested a rethink about the relation between lactic acidosis and metformin. However, they still recommended withdrawing therapy in acute renal insufficiency and when contrast dyes are used for radiological investigation. 

The pH of the plasma may be considered to be a function of two independent variables (1) the PCO2, which is regulated by the lungs and represents the acid component of the carbonic acid/bicarbonate buffer system, and (2) the concentration of titratable base (base excess or deficit, which is defined later), which is regulated by the kidneys. The plasma bicarbonate concentration is generally taken as a measure of the base excess or deficit in plasma and ECF, although it is recognized tliat conditions exist in which bicarbonate concentration may not accurately reflect the true base excess or deficit. 

Bicarbonate is the second largest fraction (behind Ci ) of plasma anions ( 25 mmol/L). Conventionally, it is defined to include (1) plasma bicarbonate ion, (2) carbonate, and (3) CO2 bound in plasma carbamino compounds (Figure 46-7). At the pH of blood, the plasma carbonate concentration is 25 pmol/L, which is -1/700 to 1/1000 of the total bicarbonate concentration. C02-bound carbamino compounds (RCNHCOOH) are 0.2 mmol/L in plasma and 1.5 mmol/L in erythrocytes. Actual bicarbonate ion concentration is not measured, but rather calculated from the Henderson-Hasselbalch equation as described below (and discussed in detail in Chapter 27). Also, as described in Chapter 27, the analyte usually measured in plasma is total COa, which includes bicarbonate and dissolved CO (dC02). The dC02 fraction is defined to include both the undissociated carbonic acid and physically dissolved, free CO2. At the pH of the blood, the amount of dissolved CO2 is 700 to 1000 times greater than the amount of carbonic acid and therefore... 

Most metabolic acid-base disorders develop slowly, within hours in diabetic ketoacidosis and months or even years in chronic renal disease. The respiratory system responds immediately to a change in acid-base status, but several hours maybe required for the response to become maximal. The maximum response is not attained until both the central and peripheral chemoreceptors are fully stimulated. For example, in the early stages of metabolic acidosis, plasma pH decreases, but because H ions equilibrate rather slowly across the blood-brain barrier, the pH in CSF remains nearly normal. However, because peripheral chemoreceptors are stimulated by the decreased plasma pH, hyperventilation occurs, and plasma PCO2 decreases. When this occurs, the PCO2 of the CSF decreases immediately because CO2 equilibrates rapidly across the blood-brain barrier, leading to a rise in the pH of the CSF. This will inhibit the central chemoreceptors. But as plasma bicarbonate gradually falls because of acidosis, bicarbonate concentration and pH in the CSF wih also fall over several hours. At this point, stimulation of respiration becomes maximal as both the central and peripheral chemoreceptors are maximally stimulated. 

Metabolic acidosis is readily detected by decreased plasma bicarbonate (or a negative extracellular base excess), the primary perturbation in this acid-base disorder. Bicarbonate is lost in the buffering of excess acid. Causes include the foUowing ... 

As the concentration of HCO3 (i.e., of metabolic CO2) in red blood cells increases, an imbalance occurs between the bicarbonate ion concentrations in the red blood cell and plasma. This osmotic imbalance causes a marked efflux of HC03 to plasma and consequent influx of Cl from plasma in order to maintain the balance of electrostatic charges. The latter osmotic influx, known as the chloride shift, is accompanied by migration of water to red blood cells. Thus, transport of metabolic CO2 in the blood occurs primarily in the form of plasma bicarbonate formed after CO2 diffuses into red blood cells. 

Asymptomatic patients with mild to moderate degrees of acidemia (plasma bicarbonate of 12 to 20 mEq/L pH of 7.2 to... 

The management of patients with life-threatening acute metabolic acidosis (plasma bicarbonate of 8 mEq/L and pH... 

Metabolic alkalosis is a simple acid-base disorder that presents as al-kalemia (increased arterial pH) with an increase in plasma bicarbonate. It is an extremely common entity in hospitalized patients with acid-base disturbances. Under normal circumstances, the kidney is readily able to excrete an alkali load. Thus evaluation of patients with metabolic alkalosis must consider two separate issues (1) the initial process that generates the metabolic alkalosis and (2) alterations in renal function that maintain the alkalemic state. °... 

The combination of respiratory and metabolic alkalosis is the most common mixed acid-base disorder. This mixed disorder occurs frequently in critically ill surgical patients with respiratory alkalosis caused by mechanical ventilation, hypoxia, sepsis, hypotension, neurologic damage, pain, or drugs, and with metabolic alkalosis caused by vomiting or nasogastric suctioning and massive blood transfusions. It may also occur in patients with hepatic cirrhosis who hyperventilate, receive diuretics, or vomit, as well as in patients with chronic respiratory acidosis and an elevated plasma bicarbonate concentration... 

This mixed disorder is often seen in patients with advanced liver disease, salicylate intoxication, and pulmonary-renal syndromes. The respiratory alkalosis decreases the PaC02 beyond the appropriate range of the respiratory compensation for metabolic acidosis. The plasma bicarbonate concentration also falls below the level expected in compensation for a simple respiratory alkalosis. In a sense, the defense of pH for either disorder alone is enhanced thus the pH may be normal or close to normal, with a low PaC02 and a low [HCOj]. Treatment of this disorder should be directed at the underlying cause. Because of the enhanced compensation, the pH is usually closer to normal than in either of the two simple disorders. 

This mixed disorder often occurs in patients with chronic obstructive pulmonary disease and chronic respiratory acidosis who are treated with salt restriction, dinretics, and possibly glncocorticoids. When diuretics are initiated, the plasma bicarbonate may increase because of increased renal bicarbonate generation and reabsorption, providing mechanisms for both generating and maintaining metabolic alkalosis. The elevated pH diminishes respiratory drive and may therefore worsen the respiratory acidosis. 

Mild hyperventilation occurs from early pregnancy, probably due to a centrally mediated effect of progesterone, and PCO. falls. However, blood hydrogen ion concentration is maintained within non-pregnant limits, since the plasma bicarbonate falls due to an increased renal excretion of bicarbonate. Oxygen consumption increa.scs by about 2091, but PO, is relatively unchanged. 

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