Blood base excess

As in plasma, CO2 equilibration of whole blood depends on the buffer value of nonbicarbonate buffers. Thus CO2 equilibration in whole blood is dependent on hemoglobin concentration and also on pH and oxygenation status. It is possible to derive an approximate equation for whole blood CO2 equilibration and calculation of whole blood base excess as follows ... 

ApH = measured pH - the standard pH of 7.40 AcB (B) the whole blood base excess (i.e., the concentration of titratable base when titrating the blood with strong acid or base to pH = 7.40 at PCO2 IStd] and 37 C)... 

This equation for whole blood base excess (Icnown as the Van Slyke equation ), together with the Henderson-Hasselbalch equation, provides the simplest algorithm for calculation of the various acid-base variables. The buffer... 

If heparin comprises 10% or more of the total volume of a sample for blood gas analysis, errors in measurements of carbon dioxide pressure, bicarbonate concentration, and base excess may occur. 

A 15-year-old girl took 38 g of metformin (135). Her pH was 7.29, bicarbonate 17 mmol/1, base excess -10 mmol/1, and blood glucose 9.2 mmol/1 after receiving glucose from the rescue team. Her condition worsened—the bicarbonate fell to 15 mmol/1, the pH to 7.2, and the blood glucose to 2.7 mmol/1 the lactate rose to 8.7 mmol/1. The lactate concentration subsequently peaked at 21 mmol/1. 

The treatment of acid-base disturbances should be directed at the imderlying cause and the specific plasma constituent imbalance. It is possible to determine the relative contributions of sodium, chloride, unidentified anions (principally lactate in horses) and protein to the metabolic component of acid-base disturbances by the use of equations based on the calculated base excess (Corley Marr 1998, Whitehair et al 1995). However, decisions on treatment can often be based on the absolute values of these blood constituents and it is only in complex disturbances, with changes in multiple plasma constituents, that the equations are usually necessary. 

If any two of the variables are known, the third can always be calculated. Indeed, blood gas analyzers (Fig. I) are programmed to provide this information which is printed out on the report I orni and usually includes the measured POi us well. There are a multitude of other calculated values oit some blood gas analyzer print outs, such as base excess and standard bicarbonate. These nitty be mostly disregarded in the routine assessment of a patient s acid-base balance. 

In a randomized, double-blind comparison of boluses of phenylephrine 100 micrograms and ephedrine 10 mg for hypotension (systolic blood pressure below lOOmmHg) in 204 patients undergoing cesarean section under spinal anesthesia, umbilical arterial and venous pH and base excess were similar in the two groups [32 ]. In those who received ephedrine umbilical arterial and venous lactate concentrations were slightly higher and more patients had nausea or vomiting (13% versus 3.9%). Clinical neonatal outcomes were similar. The authors concluded that phenylephrine and ephedrine are both suitable vasopressors for use in non-elective cesarean sections. 

In 90 women who underwent cesarean deliveries under spinal anesthesia, phenylephrine, phenylephrine + ephedrine, and ephedrine were used to maintain the blood pressure near baseline by adjusting the infusion rates [40 f. Fetal heart rates increased significantly after infusion of phenylephrine - -ephedrine and ephedrine alone but did not change after phenylephrine alone. After ephedrine, umbilical arterial and venous pH and base excess were lower than after phenylephrine alone and phenylephrine + ephedrine. Umbilical arterial PCO2 and plasma concentrations of lactate and glucose after ephedrine were greater than after phenylephrine. The authors concluded that phenylephrine may be better than ephedrine for treating the hypotension of spinal anesthesia for cesarean delivery. 

Base excess is a calculated value representing the amount of buffering anions in the blood (primarily HCO3 but also hemoglobin, proteins, phosphates, and others). The normal range of base excess is 2 mEq/L. A negative base excess (-3 mEq/L or less) indicates a deficit of base and a metabolic acidosis (i.e., ketoacidosis or lactic acidosis). A positive base excess (3 mEq/L or more) indicates metabolic alkalosis (may be present in compensation for a respiratory acidosis). 4... 

The change in acid-base status in uncompensated metabolic alkalosis is represented by the move from point N to point C in Figure 4.1. The increase in bicarbonate concentration is evident from the upward movement. This point C has a PcOj coordinate of 40mmHg, so the value of the bicarbonate at this point is also the standard bicarbonate for this sample of blood. The rise in standard bicarbonate only estimates the contribution of the COj-bicarbonate system (reaction 2 in Table 4.2A), ignoring that of the non-bicarbonate buffer (reaction 1 in Table 4.2A). The relative amount of buffering provided by the two systems varies in different conditions. To measure the excess alkali in blood at point C, it is necessary to measure the increase of both [Pr ] and [HCO3 ] in the blood. This is called the base excess. To measure the base excess directly, back titration must be used. 

The base excess is the change from normal of the sum of the concentration of bicarbonate and non-bicarbonate buffer base ([HCO3"]-K [Pr ]). The steps involved in the measurement are shown in Table 4.2B. The first step is to take a measured volume of the patient s blood and to equilibrate it at 37°C with a gas mixture containing carbon dioxide at a partial pressure of 40 mmHg. This removes any respiratory component of the acid base disorder. 

Figure 4.2. Graph to show the regions of the acid-base status plot corresponding to positive and to negative base excess. The unshaded area around the normal blood line gives an approximate indication of the variations in base excess to be found in a normal healthy population.

In the initial stages of a disturbance of acid-base physiology, the condition is uncompensated, which essentially means that chemical buffering alone is operating. At this stage therefore, there is only one component to the disorder. This component is respiratory in respiratory disorders and metabolic in metabolic disorders. In the respiratory disorder the subject moves along the normal blood line. The partial pressure of carbon dioxide is abnormal but the base excess, the measure of metabolic component, is zero. This is shown in Table 4.4A. For an uncompensated metabolic disorder (Table 4.4C), it is the... 

Compensation renders the situation more complex. In respiratory acidosis, for instance, compensation involves the retention of bicarbonate by the kidneys as illustrated in Figure 3.1. This results in the subject moving to a new blood line indicating the addition of a metabolic component to an initially purely respiratory effect. The compensation means that there is now a positive base excess in addition to the raised partial pressure of carbon dioxide. So in compensated respiratory acidosis, there are both resjnratory and metabolic components. The respiratory component is the primary disorder and the metabolic component is the secondary effect. The primary respiratory component is in the direction of acidaemia and the secondary metabolic response component is in the direction of restoration of pH, i.e. in the direction of alkalaemia. In compensation, therefore, as shown in Table 4.4B, both the partial pressure of carbon dioxide and the base excess are raised. 

This section considers the Siggaard-Andersen nomogram for reading off the parameters of acid base status such as the base excess. It has previously been noted that, although the PCO2 and [HCOj"] values for a sample of arterial blood define a point on the chart of acid-base status, they do not by themselves provide enough information to identify the magnitude of the base excess, total... 

A strong acid, such as hydrochloric acid, is now added to normal blood and to normal separated plasma. In each case, 20 mM acid is added to one litre of blood or plasma. Each fluid now has a base excess of — 20mM. Next both fluids are equilibrated with a gas mixture containing carbon dioxide at a partial pressure of 40 mmHg and the pH values are measured. Although the blood is a good buffer, its pH falls its status is shown by point A in Figure 4.7. 

The separated plasma is an inferior buffer so that the pH falls further than for blood the status of the acidotic plasma is shown by point B in Figure 4.7. If the PCO2 is varied and the resultant pH is measured, each fluid gives a relationship similar to that of its partner obtained before adding the strong acid but now the two lines cross at point C, with a value of Pcoj below 40 mmHg. This point is labelled — 20, to indicate the base excess of this blood and plasma. 

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