Normal buffer base

When blood is taken from a patient for examination of acid-base status, the haemoglobin concentration of the blood is also measured routinely. Blood from an anaemic patient, being less well buffered than normal blood, yields a line on the Siggaard-Andersen plot with a slope nearer to - 1 than normal blood. To calculate the contribution of the anaemia, it is necessary to introduce the concept of normal buffer base . The normal buffer base of a sample of... 

To estimate the normal buffer base for a sample of blood giving a particular blood line, the procedure is to read off the corresponding base excess and the... 

Observed buffer base = normal buffer base + observed base excess. 

Normal buffer base = observed buffer base — observed base excess. 

This last formula allows one to calculate the normal buffer base from values read from the Siggaard-Andersen nomogram. This normal buffer base value is then identified on the part of the buffer base curve against which is plotted the haemoglobin subscale and the haemoglobin is read off. 

For this patient, the normal buffer base is 56 —10 = 46 mM. On the full Siggaard-Andersen chart of Figure 4.9, the haemoglobin value is read as 10 g%. 

Define normal buffer base, describe how to calculate it and explain its value. 

Normal buffer base (NBB) The concentration of buffer base when any changes in the magnitude of the buffer base contributed by disturbance of acid-base status have been removed. NBB = BB — BE. 

The increase or appearance of peaks has several possible explanations. Addition of contaminants by the base during extraction is minimal, as proven by GC analysis of blank ether extractions of the buffer used in the procedure. The base could convert compounds and thus account for some of the new peaks seen. However, the hump obscures the normal column base line, and the removal of the hump by base extraction may cause previously undetected or unintegrated compounds to be measured. The hump-associated retention times have more detector noise than the other retention times in the chromatograms. The integrator usually defines the detector noise as a peak unless the sensitivity of the integrator is decreased (22). 

Mark the point at which pH 7.2 corresponds to [HC03 ] = 18.5 (at the pC02 = 50 mm isobar). Now draw a line parallel to the normal buffer line through this point. It intersects the pH 7.4 line at the 15 meq/L point. Base deficit is 24 (normal) - 15 = 9 meq/L. 

Adults and older children tend to correct the disturbance at this point. Young children, however, quickly develop a fall in the blood pH (metabolic acidosis), due to salicylate stimulation of metabolism. The toxic effects of salicylate and the loss of buffer base interfere with metabolic processes, and ketosis develops. Because the respiratory alkalosis and metabolic acidosis occur simultaneously, a child may present with a mixed disturbance and a relatively normal pH, or with frank acidosis. The PC02 will be lower than expected. Children < 4 yr develop metabolic acidosis more rapidly, without concurrent respiratory alkalosis. Dehydrationj is a serious problem because of insensible water loss and increased renal water loss (from an increased urine solute load). Severe losses of sodium and potassium are not uncommon (15). 

Normalized p values for this reaction catalyzed by three different aryloxide ions are reported in Table 12 while Brpnsted coefficients for this type of catalysis are summarized in Table 13. The rather low values (high a(k )) suggest that the proton transfer from the attacking methanol nucleophile to the buffer base has made much less progress than the C-0 bond formation at the transition state (or that in the reverse direction protonation of the departing MeO by the buffer acid is ahead of C-0 bond cleavage), as shown in 82 on MeO group). 

The need for a better measure of the metabolic component of an acid-base disorder. At first sight, w e might think that the deviation of the standard bicarbonate from the value for normal blood is all the information that we need about the non-respiratory component of an acid- base disorder. However, the change in standard bicarbonate underestimates the non-respiratory component of the acid base disorder. To illustrate this, consider uncompensated metabolic alkalosis, produced by the addition of alkali, such as sodium hydroxide, to the blood. Each of the buffer acids in the blood (protein buffer acid and CO2) buffers some of the added alkali as shown in the two chemical reactions in Table 4.2A. Protein buffer acid combines with some of the alkali to yield water and protein buffer base CO2 from metabolism combines with most of the rest of the alkali to yield bicarbonate. The result is an increase in concentration both of non-bicarbonate buffer base Pr and of bicarbonate. 

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. 

The summed concentration of bicarbonate and non-bicarbonate buffer base ([HC03 ] + [Pr ]) is called the total buffer base or, more usually, the buffer base (Table 4.3A). For blood of normal composition in equilibrium with gas... 

A. Buffer Base (or Total Buffer Base) is ([HCOa ] + [Pr ]) Typical value for normal blood is 48 mM. 

The concentration of total buffer base depends on the overall buffering power of the blood. Since much of the buffering is due to haemoglobin, in an anaemic person the total buffer base is low. An anaemic person with no disturbance of acid-base physiology will normally operate at a normal PCO2 and normal... 

Figure 4.3. A. Normal blood the normal blood line is plotted with axes as indicated below and to the left. The full arrows show the value of the [HCOj j at the relevant PtU2. Above each full arrow is a dashed arrow indicating the concentration of non-bicarbonate buffer base. The two arrows together indicate the magnitude of the total buffer base. B. A similar plot for anaemic blood.

The basic deficiency is the lower-than-normal concentration of non-bicarbonate buffer base. When the PcOj with which the blood is equilibrated is changed, the inferior buffering power of anaemic blood is expressed. The slope of the blood line is less than for non-anaemic blood (Figure 4.3B). This is matched by lower values for non-bicarbonate buffer base at all PcOj values. Correspondingly, the total buffer base is less than 48 mM, because of a relative lack of non-bicarbonate buffer base. 

Next to be considered are the anions. Since, in acid-base physiology, buffer base is of prime importance, it is sited at the top of the bar graph. Protein buffer base at 15 mequiv./litre and bicarbonate at 24 mequiv./litre are shown. These values for Pr and HCOj correspond to a normal [H" ] of 40 nM (pH 7.4) and a normal arterial PCO2 of 40 mmHg. Next chloride, the principal anion, is shown with a concentration of around 1(X) mequiv./litre. The remainder, comprising sulphate etc., add up to 11 mequiv./litre. 

The value given for the total buffer base for plasma (taken from Figure 5.2) is (15-1- 24), i.e. typically 39 mM whereas that for whole blood is typically 48 mM. Whole blood is a better buffer than plasma, principally because of the haemoglobin contribution to buffering, which is why it has a larger concentration of total buffer base. It has already been noted that anaemic blood has a reduced amount of buffer base, reflecting the poorer buffering capacity by comparison with normal blood. 

E. At point B, the total buffer base is above normal. 

E. Yes. Any point above the normal blood line has an increased value of total buffer base. 

We have known the ojj t setup time Ts 70s in subsection 4.1.2. For Csdi, we use switch thre old factor =Csdilr instead of Csch- The calculation of CgOt is a litter fussy, referring to Fig.9 i). let Csd,=kVJ,(f) just before the first jump of Wp t) ii). Let Cxh=Vp t) just after the first big change in dVp f)/dt in), let Csch =mean of Vp f) on its flat part iv). let Csdi=Vp(t) just before the jump of Vp t). The results of all above methods are plotted in Fig.lO, and we have jS=90s. Next, W is deduced from our crawler trace. Based on the statistics over total 15,831 peers lasting for at least 5 minutes since they entered stable state, we get a similar result for both normalized buffer width and offset lag relative to s(t). At last, the relative initial offset is figured out from sniffer trace. The distribution of W and Op are shown in Fig.ll. Based on our measurement, we have lV 210s and 0p = 70s. 

A pH electrode is normally standardized using two buffers one near a pH of 7 and one that is more acidic or basic depending on the sample s expected pH. The pH electrode is immersed in the first buffer, and the standardize or calibrate control is adjusted until the meter reads the correct pH. The electrode is placed in the second buffer, and the slope or temperature control is adjusted to the-buffer s pH. Some pH meters are equipped with a temperature compensation feature, allowing the pH meter to correct the measured pH for any change in temperature. In this case a thermistor is placed in the sample and connected to the pH meter. The temperature control is set to the solution s temperature, and the pH meter is calibrated using the calibrate and slope controls. If a change in the sample s temperature is indicated by the thermistor, the pH meter adjusts the slope of the calibration based on an assumed Nerstian response of 2.303RT/F. 

The differences in the amino acid chemistry of the hide coUagen and the hair keratin are the basis of the lime-sulfide unhairing system. Hair contains the amino acid cystine. This sulfur-containing amino acid cross-links the polypeptide chains of mature hair proteins. In modem production of bovine leathers the quantity of sulfide, as Na2S or NaSH, is normally 2—4% based on the weight of the hides. The lime is essentially an unhmited supply of alkah buffered to pH 12—12.5. The sulfide breaks the polypeptide S—S cross-links by reduction. Unhairing without sulfide may take several days or weeks. The keratin can be easily hydrolyzed once there is a breakdown in the hair fiber stmcture and the hair can be removed mechanically. The coUagen hydrolysis is not affected by the presence of the sulfides (1—4,7). 

Based on the above equilibria, the concentration of HOCl in the normal pH range varies inversely with the total concentration of cyanurate. Increased concentration of cyanuric acid, therefore, should decrease the biocidal effectiveness of FAC. This has been confirmed by laboratory studies in buffered distilled water which showed 99% kill times of S.faecalis at 20°C increasing linearly with increasing cyanuric acid concentration at constant av. Cl at pH 7 and 9 (45). Other studies in distilled water have found a similar effect of cyanuric acid on kill times of bacteria (46—48). Calculations based on the data from Ref. 45 show that the kill times are highly correlated to the HOCl concentration and poorly to the concentration of the various chloroisocyanurates, indicating that HOCl is the active bactericide in stabilized pools (49). 

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