Respiratory Acidosis. The decision to ventilate a patient to reduce the PCO2 is a clinical decision and is based on exhaustion, prognosis, prospect of improvement from concurrent therapy, and in part on the PCO2 level. Once the decision is made, the PCO2 helps to calculate the appropriate correction. The PCO2 reflects a balance between the carbon dioxide production and its elimination. Unless the metabolic rate changes, the amount of carbon dioxide to be eliminated remains constant. It directly determines the amount of ventilation required and the level of PCO2. Where VT equals tidal volume and f equals respiratory rate:
PCO2 x Ventilation = Constant, i.e.,
PCO2 x VT x f = k
This equation means that the same number of carbon dioxide molecules can be eliminated by high ventilation at a low PCO2 or by low ventilation at a high PCO2. A new PCO2 can be achieved by selecting a ventilation such that the product of the two again produces the same constant. For example, if the PCO2 is 60 and the ventilation is 4 L/min (4 x 60 = 240), then to achieve a PCO2 of 40, the ventilation should be increased to 6 L/min (6 x 40 = 240). In general, it is safe to return acute disturbances towards normal. With chronic disturbances, e.g., chronic respiratory failure, it may be wiser to be cautious and aim for the patient's customary PCO2 which may be considerably higher than 40 mmHg.
Metabolic Acidosis. The treatment for a metabolic acidosis is, again, judged largely on clinical grounds. Bicarbonate therapy is justified when metabolic acidosis accompanies difficulty in resuscitating an individual or in maintaining cardiovascular stability. A typical dose of bicarbonate might be 1 mEq per kilogram of body weight followed by repeat blood gas analysis. The effect of a dose of bicarbonate can be anticipated by calculating the dose required for complete correction. A lesser dose has proportionately less effect. This calculation is based on BE and the size of the treatable space (0.3 x weight, e.g., 21 liters, see above under Physiology):
Dose (mEq) = 0.3 x Wt (kg) x BE (mEq/L)
The dose calculated will be sufficient to return the metabolic disturbance to about zero. This complete dose is very rarely recommended. As described above, it is customary to either give a small standard dose and reevaluate; or give about half the calculated dose. There are several reasons for this caution:
1. Bicarbonate is, initially, injected into the plasma volume, about 3 liters, instead of into the calculated treatable space, 21 liters.
2. When bicarbonate is added to acid it "fizzes". Fortunately this does not occur literally in the blood. Nevertheless, the majority of the bicarbonate is converted to carbon dioxide and has to be eliminated. For each 100 mEq which is converted, about 2.24 liters of carbon dioxide has to be exhaled, equivalent to ten minutes normal production.
3. The carbon dioxide which is produced enters the cells freely, unlike the bicarbonate ions which have been administered. Therefore, the inside of the cell should initially become more acid. However, direct studies employing nuclear magnetic resonance have not confirmed this (Severinghaus, Personal Communication 1986).
4. The bicarbonate is accompanied by sodium ions which will increase the osmolality of the extracellular fluid. In combination with other therapy, such as intravenous glucose, the hyperosmolality may be critical and cause coma. In neonates, rapid infusion of bicarbonate may cause intracranial hemorrhage.
5. After the body has dealt with its metabolic acidosis there is a residual metabolic alkalosis, hypernatremia, and hyperosmolality.
Anion Gap. Some causes of metabolic acidosis release anions into the extracellular fluid which are not normally measured. When this occurs there will be an unexpected discrepancy between the sums of the principal cations and anions. The usual sum is:
Na+ (140)+ K+ (5) = C1- (105) + HCO3- (25) + Gap (15)
When there are any additional, unmeasured anions, they become part of the "gap" which is, then, correspondingly larger. A gap greater than 30 suggests that there is an increase in the concentration of the unmeasured anions. Unfortunately, this method relies upon the accuracy of the other measurements. Small errors in the larger numbers causes a proportionately greater error in the result. If information is required about the anions, it is more appropriate to measure their concentration. In practice it suffices to analyze lactate in tissue hypoxia, 3-hydroxybutyrate in diabetic ketosis, and phosphate or sulfate in renal failure.
Nevertheless, there are circumstances when it is necessary to know the value of the PCO2 at the cooled temperature. If the arterial values are being compared to gases being exhaled or to the gases in a pump-oxygenator, then the arterial values must be calculated for the low temperature. In most circumstances, however, this calculated value is hard to evaluate because it is unfamiliar and correspondingly difficult to interpret.
One pascal is one newton per square meter. One newton is about 102 grams weight or about 3.6 ounces of fluid. Therefore, when one newton (a small cup of coffee) is spilled on to a table one meter square, the resulting layer of water (0.102 mm H2O) is equivalent to one pascal. A pressure of one thousand pascals (1 kPa) is about 10.2 cm H2O or about 7.75 mmHg. Atmospheric pressure is about 1000 cm H2O (1034) or 100 kPa (101.9). To convert pressure in mmHg to kPa, it is necessary to divide the value in mmHg by 7.5.
If the sum of PO2 + PCO2 is greater than expected, then the analysis contains an error. A sum which is smaller suggests that the lungs are failing to adequately transfer oxygen. For greater accuracy, this sum must incorporate the respiratory quotient (RQ). Then, at atmospheric pressure breathing room air, the corrected sum of the respiratory gases in the alveoli is 150 mmHg:
PO2 + PCO2 / RQ = 150 mmHg
This degree of accuracy is not required for most purposes. Moreover, the RQ is frequently unknown. Accordingly it is simpler and reasonably accurate to add the PCO2 and PO2 directly:
PO2 + PCO2 = 140 mmHg
Variation in the pH alters the degree of ionization of proteins and many drugs. As most ionized substances do not cross cell membranes readily, alterations in pH affect both cellular function and the potency of many pharmaceutical agents. Relative acidity of tissues, for example in the vicinity of an abscess, is recognized to reduce the efficacy of local anesthetic solutions. Conversely, relative alkalinity enhances the uptake of local anesthetic solutions. Alkalinity also potentiates drugs such as meperidine and morphine by increasing the availability of lipophilic, uncharged base, to cross the blood-brain barrier (Shulman et al 1984).