Respiratory alkalosis chronic

Chronic respiratory alkalosis t Decreased3 Decreased0 AHCO3- = 0.4 x ARaC02d... 

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). 

The symptoms produced by respiratory alkalosis result from increased irritability of the central and peripheral nervous systems. These include light-headedness, altered consciousness, distal extremity paresthesias, circumoral paresthesia, cramps, carpopedal spasms, and syncope. Various supraventricular and ventricular cardiac arrhythmias may occur in extreme cases, particularly in critically ill patients. An additional finding in many patients with severe respiratory alkalosis is hypophosphatemia, reflecting a shift of phosphate from the extracellular space into the cells. Chronic respiratory alkalosis is generally asymptomatic. 

Baseline and periodic serum bicarbonate levels to monitor for hyperchloremic, nonanion gap metabolic acidosis (i.e., decreased serum bicarbonate below the normal reference range in the absence of chronic respiratory alkalosis)... 

As with the metabolic acid-base disturbances, there are two cardinal respiratory acid-base disturbances respiratory acidosis and respiratory alkalosis. These disorders are generated by a primary alteration in carbon dioxide excretion, which changes the concentration of carbon dioxide, and therefore the carbonic acid concentration in body fluids. A primary reduction in PaC02 causes a rise in pH (respiratory alkalosis), and a primary increase in PaC02 causes a decrease in pH (respiratory acidosis). Unlike the metabolic disturbances, for which respiratory compensation is rapid, metabolic compensation for the respiratory disturbances is slow. Hence these disturbances can be further divided into acute disorders, with a duration of minutes to hours that is too short for metabolic compensation to have occurred, and chronic disorders, that have been present long enough for metabolic compensation to be complete. 

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... 

All patients developed a compensatory metabolic acidosis due to chronic hyperventilation. Respiratory alkalosis was thought to have developed because of capillary leak into the lungs producing borderline or frank pulmonary edema. After several days a superimposed normal anion gap acidosis developed from dilution by large volumes of saline fluid resuscitation. The authors found no defects in renal handling of calcium, phosphorous, or magnesium. There was no evidence of a renal acidification defect or renal tubular acidosis. 

The concentration of CO2 in blood is usually represented as FCO2, the partial pressure of CO2. Bicarbonate concentration can be regarded as the metabolic component of acid-base homeostasis while CO2 can be regarded as the respiratory component. Thus a primary change in one of these components as a result of a clinical condition can result in a compensatory change in other component. Raised blood PCO2 occurs in respiratory acidosis (as in chronic obstructive airway disease] and compensated metabolic alkalosis. Low blood PCO2 is found in respiratory alkalosis (hyperventilation) and in compensated metabolic acidosis. 

Rarely, may lead to a small rise in PC02 in patients with chronic respiratory acidosis ° If alkalosis persists or if pH > 7.6 or HC03 >45 mEq/L... 

Metabolic alkalosis and respiratory acidosis can occur in patients with chronic obstructive pulmonary disease and respiratory acidosis who are treated with salt restriction, diuretics, and possibly glucocorticoids. 

Acetazolamide can cause a metabolic acidosis in 50% of elderly patients (SEDA-11,199) occasionally (particularly if salicylates are being given or renal function is poor) the acidosis can be severe. It does this by inhibiting renal bicarbonate reabsorption. This effect is of particular use in treating patients with chronic respiratory acidosis with superimposed metabolic alkalosis. Life-threatening metabolic acidosis is rarely observed in the absence of renal insufficiency and/or diabetes mellitus. In three patients with central nervous system pathology alone conventional doses of acetazolamide resulted in severe metabolic acidosis (34). After withdrawal it took up to 48 hours for the metabolic acidosis and accompanying hyperventilation to resolve. 

Figure 3.4 Identification of various acid-base disturbances. Acute disorders are synonymous with uncompensated disturbances, whereas chronic conditions are synonymous with partially compensated or compensated disturbances. If a specific case falls outside the shaded areas, a compound acid-base disturbance may be suspected, such as the coexistence of respiratory acidosis (partially compensated) and metabolic alkalosis. Unshaded areas may also indicate a transient state between an acute (uncompensated) state and a chronic (partially compensated) condition. (From Cogan MG, Rector FC Jr., Seldin DW. In Brenner BM, and Rector FC Jr, eds. The Kidney, 2nd ed., Vol. 1, Philadelphia WB Saunders, 1986, p. 860.)...

Hjqiochloremia is common in gastrointestinal disease (Svendsen et al 1979), because of the loss of gastric hydrochloric acid in high volume reflux from the stomach (in proximal enteritis and grass sickness) and the secretion and/or lack of absorption of chloride in severe colitis. It may also occur in exhausted horse syndrome, chronic compensated respiratory acidosis and following furosemide (frusemide) administration. Hypochloremia in the absence of hyponatremia results in a metabolic alkalosis (Corley Marr 1998). The alkalosis associated with hypochloremia may also result in increased cellular uptake of potassium, leading to hypokalemia (Schaer 1999). 

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. 

Chronic pulmonary failure may be further complicated by metabolic disturbances tending to metabolic alkalosis or metabolic acidosis. The mechanism leading to alkalosis is not always clear, but among the factors that may influence it are the loss of hydrogen and Cl ions, because of vomiting or because of selective Cl and potassium depletion as a result of undernourishment, and prolonged treatment with diuretics. It is usually assumed that severe respiratory acidosis is always accompanied by metabolic acidosis. This reasoning is based on the fact that when the same CO2 tensions are achieved in the blood in vivo and in vitro,the plasma concentration of bicarbonate for identical pH s is lower in vivo than in vitro. In reality, this bicarbonate deficit seems to result because (I) the buffer curve of the blood CO2 has a lower slope in vivo than in vitro and (2) hyperventilation in vivo leads to lactic acid accumulation in he blood. 

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