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Ácido-Base

Ácido-Base

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Art. Medicina, Principios Acido- Base
Art. Medicina, Principios Acido- Base

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Published by: José Daniel Moreno A. on Dec 28, 2012
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6
Review
Determinants of blood pH in health and disease
John A Kellum
University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA
 Abstract
An advanced understanding of acid–base physiology is as central to the practice of criticalcare medicine, as are an understanding of cardiac and pulmonary physiology. Intensivistsspend much of their time managing problems related to fluids, electrolytes, and blood pH.Recent advances in the understanding of acid–base physiology have occurred as the resultof the application of basic physical-chemical principles of aqueous solutions to bloodplasma. This analysis has revealed three independent variables that regulate pH in bloodplasma. These variables are carbon dioxide, relative electrolyte concentrations, and totalweak acid concentrations. All changes in blood pH, in health and in disease, occur throughchanges in these three variables. Clinical implications for these findings are also discussed.
Keywords:
acid–base balance, acidosis, alkalosis, anion gap, arterial blood gases, strong ion difference, strongion gapReceived: 29 November 1999Accepted: 30 November 1999Published: 24 January 2000
Crit Care
2000,
4
:6–14© Current Science LtdAG = anion gap; A
TOT
= total weak acid concentration; SBE = standard base excess; SID = strong ion difference; SIG = strong ion gap; pCO
2
,partial carbon dioxide tension.http://ccforum.com/content/4/1/006
Introduction
Whereas most medical and surgical subspecialistsconcern themselves with a specific organ (eg nephrology),region of the body (eg cardiothoracic surgery), or diseaseprocess (eg infectious disease), practitioners of criticalcare are more often concerned with the interaction ofvarious organs and disease states. As such, our practice isoften defined by certain syndromes (sepsis, multiorganfailure) and pathophysiologic conditions (shock) that do notconfine themselves to the domains of a single subspecialty.Acid–base regulation is one of these ‘areas’ of medicinethat crosses organ-specific boundaries, and the intensivecare unit is often the place where severe derangements inthis area exist. For these reasons, intensivists, and otherscalled upon to care for critically ill patients in the intensivecare unit, operating room, or emergency department, areexpected to diagnose and manage complicated disordersof acid–base balance. This review provides a rather in-depth examination of chemistry and physiology of acid–base balance in health and disease.The concentration of H
+
in blood plasma and various otherbody solutions is among the most tightly regulated vari-ables in human physiology. (Most of the principles dis-cussed in this review are applicable to animal physiologyas well. A complete discussion of the differences betweenspecies, however, particularly aquatic versus terrestrialspecies, is beyond the scope of the present review.)Acute changes in blood pH induce powerful regulatoryeffects at the level of the cell, organ, and organism [1].
 
http://ccforum.com/content/4/1/0067
 
The mechanisms responsible for local, regional, and sys-temic acid–base balance are incompletely understoodthough, and controversy exists in the literature as to whatmethods should be used to understand these mecha-nisms [2]. Much of this controversy exists only becausethe strict rules for causation (as opposed to correlation)have not often been applied to the understanding ofacid–base balance, and methods that are useful clinicallyhave often been used to understand physiology withoutbeing subjected to appropriate scientific rigor. The use ofvarious laboratory variables to diagnose an acid–base dis-order is analogous to the use of the electrocardiogram todiagnose a myocardial infarction. However, neither thechanges in the electrocardiogram tracing nor the distur-bances in electrical conduction that these changes reflectwere ever considered to be the cause of a myocardialinfarction. In contrast, changes in HCO
3
(bicarbonate)concentration, for example, have been assumed to beresponsible for metabolic acidosis or alkalosis. Failure toestablish causation has lead to numerous incorrectnotions of acid–base physiology and has fueled years of,often heated, debate [2–4]. This review analyzes what isknown about the causal relationships between acid–basevariables and acid–base balance in health and disease.
Quantification, classification, and causation
In order to understand acid–base physiology, we mustfirst agree on how to describe and measure it. SinceSörensen (1868–1939) first introduced the pH notation,we have used the pH scale to quantify acid–base balanceThe pH scale has a tremendous advantage because itlends itself to colorimetric and electrometric techniques.There is also some physiologic relevance to the logarith-mic pH scale [5]. pH is a confusing variable, however. It isa nonlinear transformation of H
+
concentration – the loga-rithm of its reciprocal. Strictly speaking, pH can only bethought of as a dimensionless representation of H
+
con-centration and is not, itself, a concentration. Indeed, pH isactually the logarithmic measure of the volume required tocontain 1mol/l of H
+
. In blood plasma at pH7.4, thisvolume is approximately 25million liters [6].Regardless of how we express the concentration of H
+
,either directly or as the pH, it is generally accepted thatchanges in blood H
+
concentration occur as the result ofchanges in volatile [partial carbon dioxide tension (pCO
2
)]and nonvolatile acids (hydrochloric, sulfuric, lactic, etc).Clinically, we refer to changes in volatile acids as ‘respira-tory’ and changes in nonvolatile acids as ‘metabolic’.There are three major methods of quantifying (describing)acid–base disorders, and each differs only in assessmentof this latter, ‘metabolic’ component. These three methodsquantify the metabolic component either by using HCO
3
(in the context of pCO
2
), the standard base excess (SBE),or the strong ion difference (SID). Although there hasbeen significant debate regarding the accuracy and utilityof each method compared with the others, all three yieldvirtually identical results when used to quantify theacid–base status of a given blood sample [7,8]. The onlydifferences between these three approaches are concep-tual (ie in how they approach the understanding of mecha-nisms) [9–11].
Beyond Henderson and Hasselbalch
Since Hasselbalch adapted the Henderson equation to thepH notation of Sörenson, we have used the following equa-tion to understand the relationship between respiratory andmetabolic acid–base variables:pH = pK × log[HCO
3
/(0.03 × pCO
2
)](1)This is the Henderson–Hasselbalch equation, and it isimportant to realize what this equation tells us. Anincrease in pCO
2
will result in a decrease in the pH and anincrease in the HCO
3
concentration. Thus, a patientfound to have a low blood pH, a condition known asacidemia, will either have an increased pCO
2
or a pCO
2
that is ‘not increased’. In the former circumstance, weclassify the disorder as a ‘respiratory acidosis’. We usethe term ‘acidosis’ to describe the process resulting inacidemia and ‘respiratory’ because the apparent cause isan increased pCO
2
. This is logical, because carbonic acidresults when CO
2
is added to water (or blood), and theresultant decrease in pH is entirely expected. In the lattercondition pCO
2
is not increased, and thus there cannotbe a respiratory acidosis. We therefore refer to this condi-tion as ‘metabolic’ because some nonvolatile acid must bethe cause of the acidemia. We can reverse the abovelogic and easily classify simple conditions of alkalemia aseither resulting from respiratory or metabolic alkaloses.Thus, equation 1 allows us to classify disorders accordingto the primary type of acid being increased or decreased.Over time physiology superimposes its effects on simplechemistry and the relationship between pCO
2
and HCO
3
is altered in order to reduce the alterations in pH. By care-fully examining the changes that occur in pCO
2
andHCO
3
in relationship to each, however, one can discernhighly conserved patterns. In this way rules can be estab-lished to allow one to discover mixed disorders and toseparate chronic from acute respiratory derangements.For example one such rule is the convenient formula forpredicting the expected pCO
2
in the setting of a meta-bolic acidosis [12]:pCO
2
= (1.5 × HCO
3
) + 8
±
5(2)This rule tells us what the pCO
2
should be secondary tothe increase in alveolar ventilation that accompanies ametabolic acidosis. If pCO
2
does not change enough orchanges too much, we classify the condition as a ‘mixed’disorder, with either a respiratory acidosis if the pCO
2
isstill too high, or a respiratory alkalosis if the change is too
 
Critical Care
Vol 4 No 1Kellum8
great. This rule, along with others (Table 1) has beenrecently translated to SBE terminology [7]:pCO
2
= (40 + SBE)
±
5(3)For example, consider the following arterial blood gassample: pH7.31, pCO
2
31, HCO
3
15, SBE–9.5. Equation2 tells us that the expected pCO
2
=(1.5×15)+8
±
5=30.5
±
5, and in Equation 3 the SBE added to 40 also yields30.5. The measured pCO
2
of 31mmHg is consistent with apure metabolic acidosis (ie no respiratory disorder).It is also very important to understand what the Hender-son–Hasselbach equation does not tell us. First, it doesnot allow us to discern the severity (quantity) of the meta-bolic derangement in a manner analogous to the respira-tory component. For example, when there is a respiratoryacidosis, the increase in the pCO
2
quantifies the derange-ment even when there is a mixed disorder. However, themetabolic component can only be approximated by thechange in HCO
3
. Second, Equation1 does not tell usabout any acids other than carbonic acid. The relationshipbetween CO
2
and HCO
3
provides a useful clinical ‘roadmap’ to guide the clinician in uncovering the etiology of anacid–base disorder as described above. The total CO
2
concentration, and hence the HCO
3
concentration, isdetermined by the pCO
2
, however, which is in turn deter-mined by the balance between alveolar ventilation andCO
2
production. HCO
3
cannot be regulated indepen-dent of pCO
2
. The HCO
3
concentration in the plasmawill always increase as the pCO
2
increases, but this is notan alkalosis. To understand how the pH and HCO
3
con-centration are altered independent of pCO
2
, we must look beyond Henderson and Hasselbach.
Base excess
In order to address the first ‘shortcoming’ of the Hender-son–Hasselbach equation – the inability to quantify themetabolic component – several methods have beendevised. In 1948, Singer and Hastings proposed the term‘buffer base’ to define the sum of HCO
3
plus the non-volatile weak acid buffers (A
) [13]. A change in bufferbase corresponds to a change in the metabolic compo-nent. The methods for calculating the change in bufferbase were later refined by investigators [14,15] andrefined further by others [16–18] to yield the base excessmethodology. Base excess is the quantity of metabolic aci-dosis or alkalosis, defined as the amount of acid or basethat must be added to a sample of whole blood
in vitro
inorder to restore the pH of the sample to 7.40 while thepCO
2
is held at 40mmHg [15]. Although this calculationis quite accurate
in vitro
, inaccuracy exists when applied
in vivo
inthat base excess changes with changes in pCO
2
[19,20]. This effect is understood to be due to equilibra-tion across the entire extracellular fluid space (wholeblood+interstitial fluid). When the base excess equationis modified to account for an ‘average’ content of hemo-globin across this entire space, a value of 5 g/dl is usedinstead, and this defines the SBE. It should be pointed outthat this value does not represent the true content ofhemoglobin suspended in the volume of whole bloodtogether with interstitial fluid, but rather is an empiric esti-mate that improves the accuracy of the base excess. It canbe argued that the entire extracellular fluid space isinvolved in acid–base balance, because this fluid flowsthrough blood vessles and lymphatics, mixing constantly[21]. Thus, the value of SBE is that it quantifies thechange in metabolic acid–base status
in vivo
. It is of inter-est that base excess is only accurate
in vivo
whenitassumes a constant hemoglobin concentration.However, the base excess approach does not address thesecond problem associated with using the Henderson–Hasselbach equation alone (ie it still does not tell us aboutthe mechanisms of metabolic acid–base balance). Forexample the body does not ‘regulate’ the SBE. It is not asubstance that can be excreted in the feces or reabsorbedfrom the proximal tubule. Similarly, HCO
3
is not a strong
 
Table 1Observational acid–base patterns
DisorderHCO
3
(mmol/l)pCO
2
(mmHg)SBE (mmol/l)Metabolic acidosis<22= (1.5 × HCO
3
) + 8<5= 40 + SBEMetabolic alkalosis>26= (0.7 × HCO
3
) + 21>+5= 40 + (0.6 × SBE)Acute respiratory acidosis= [(pCO
2
40)/10] + 24>45= 0Chronic respiratory acidosis= [(pCO
2
40)/3] + 24>45= 0.4 × (pCO
2
– 40)Acute respiratory alkalosis= [(40 pCO
2
)/5] + 24<35= 0Chronic respiratory alkalosis= [(40 pCO
2
)/2] + 24<35= 0.4 × (pCO
2
– 40)Compiled from various sources. The changes in SBE were taken from Schlichtig
et al 
[7]. pCO
2
, partial carbon dioxide tension; SBE, standardbase excess.

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