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Chapter: Clinical Anesthesiology: Perioperative & Critical Care Medicine: Acid-Base Management

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Body Buffers

Physiologically important buffers in humans include bicarbonate (H2CO3/HCO3−), hemoglobin (HbH/ Hb−), other intracellular proteins (PrH/Pr−), phos-phates (H2PO4−/HPO42−), and ammonia (NH3/NH4+).

Compensatory Mechanisms

Physiological responses to changes in [H +] are char-acterized by three phases: (1) immediate chemical buffering, (2) respiratory compensation (whenever possible), and (3) a slower but more effective renal compensatory response that may nearly normalize arterial pH even if the pathological process remains present.

BODY BUFFERS

 

Physiologically important buffers in humans include bicarbonate (H2CO3/HCO3−), hemoglobin (HbH/ Hb−), other intracellular proteins (PrH/Pr−), phos-phates (H2PO4−/HPO42−), and ammonia (NH3/NH4+). The effectiveness of these buffers in the various fluid compartments is related to their concentration. Bicarbonate is the most important buffer in the extra-cellular fluid compartment. Hemoglobin, though restricted inside red blood cells, also functions as an important buffer in blood. Other proteins probably play a major role in buffering the intracellular fluid compartment. Phosphate and ammonium ions are important urinary buffers.

 

Buffering of the extracellular compartment can also be accomplished by the exchange of extracel-lular H+ for Na+ and Ca2+ ions from bone and by the exchange of extracellular H + for intracellular K +. Acid loads can demineralize bone and release alka-line compounds (CaCO3 and CaHPO4). Alkaline loads (NaHCO3) increase the deposition of carbon-ate in bone.

 

Buffering by plasma bicarbonate is almost immediate, whereas that due to interstitial bicar-bonate requires 15–20 min. In contrast, buffering by intracellular proteins and bone is slower (2–4 h). Up to 50% to 60% of acid loads may ultimately be buff-ered by bone and intracellular buffers.

The Bicarbonate Buffer

 

Although in the strictest sense, the bicarbonate buffer consists of H2CO3 and HCO3, CO2 tension (Pco2) may be substituted for H2CO3 because:


This hydration of CO2 is catalyzed by carbonic anhydrase. If adjustments are made in the dissocia-tion constant for the bicarbonate buffer and if the solubility coefficient for CO2 (0.03 mEq/L) is taken into consideration, the Henderson–Hasselbalch equation for bicarbonate can be written as follows:

 


where pK′ = 6.1.

 

Note that its pK is well removed from the nor-mal arterial pH of 7.40, which means that bicar-bonate would not be expected to be an efficient extracellular buffer (see above). The bicarbonate system is, however, important for two reasons: (1) bicarbonate (HCO3) is present in relatively high concentrations in extracellular fluid, and (2) more


importantly—Paco2 and plasma [HCO3] are closely regulated by the lungs and the kidneys, respectively. The ability of these two organs to alter the [HCO3]/Paco2 ratio allows them to exert important influences on arterial pH.

 

A simplified and more practical derivation of the Henderson–Hasselbalch equation for the bicarbonate buffer is as follows:


This equation is very useful clinically because pH can be readily converted to [H+] (Table 50–2). Note that below 7.40, [H+] increases 1.25 nEq/L for each 0.01 decrease in pH; above 7.40, [H+] decreases 0.8 nEq/L for each 0.01 increase in pH.


It should be emphasized that the bicarbonate buffer is effective against metabolic but notrespiratory acid–base disturbances. If 3 mEq/L of a strong nonvolatile acid, such as HCl, is added to extracellular fluid, the following reaction takes place:

 


Note that HCO 3 reacts with H + to produce CO2. Moreover, the CO2 generated is normally elim-inated by the lungs such that Paco2 does not change. Consequently, [H+] = 24 × 40 ÷ 21 = 45.7 nEq/L, and pH = 7.34. Furthermore, the decrease in [HCO 3] reflects the amount of nonvolatile acid added.

In contrast, an increase in CO2 tension (vola-tile acid) has a minimal effect on [HCO3]. If, for example, Paco2 increases from 40 to 80 mm Hg, the dissolved CO 2 increases only from 1.2 mEq/L to 2.2 mEq/L. Moreover, the equilibrium constant for the hydration of CO 2 is such that an increase of this magnitude minimally drives the reaction to the left:

 


If the valid assumption is made that [HCO3] does not appreciably change, then

 


 

 [H+] therefore increases by 40 nEq/L, and because HCO3 is produced in a 1:1 ratio with H+, [HCO3] also increases by 40 nEq/L. Thus, extracel-lular [HCO3] increases negligibly, from 24 mEq/L to 24.000040 mEq/L. Therefore, the bicarbonate buffer is not effective against increases in Paco2, and changes in [HCO3] do not reflect the severity of a respiratory acidosis.

Hemoglobin as a Buffer

 

Hemoglobin is rich in histidine, which is an effec-tive buffer from pH 5.7 to 7.7 (pKa 6.8). Hemoglobin is the most important noncarbonic buffer in extra-cellular fluid. Simplistically, hemoglobin may be thought of as existing in red blood cells in equilibrium as a weak acid (HHb) and a potassiumsalt (KHb). In contrast to the bicarbonate buf-fer, hemoglobin is capable of buffering bothcarbonic (CO2) and noncarbonic (nonvolatile) acids:

 


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