This article is intended to provide an introduction to the physiology of acid-base balance and the many pathological conditions that are associated with. The ABC's of Acid-Base Balance. Gordon S. Sacks, PharmD. The University of Wisconsin—Madison, Madison, Wisconsin. A step-wise systematic approach can . Whatever the nature of an acid-base disturbance, the response of these mechanisms leads to the formation and extraction from the plasma of a fluid with an.
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acid-base balance within tightly controlled limits. It is not the aim of this article to review in detail the physiology of acid-base homeostasis, but to provide a. Blood Gas Analysis--Insight into the Acid-Base status of the. Patient CO2 and water form carbonic acid or H2CO3, which is in equilibrium with bicarbonate. The four recognized primary acid–base disorders comprise two metabolic disorders (acidosis any medications that affect acid–base balance.
And you can restore the balance by targeting your interventions to the specific acid-base disorder you find. Examples include hydrochloric acid, nitric acid, ammonium ion, lactic acid, acetic acid, and carbonic acid H2CO3. Examples include ammonia, lactate, acetate, and bicarbonate HCO The pH of water H2O , 7. The pH of blood is slightly alkaline and has a normal range of 7.
If the blood is acidic, the force of cardiac contractions diminishes. If the blood is alkaline, neuromuscular function becomes impaired. A blood pH below 6. See Fast facts on acid-base balance by clicking the PDF icon above.
These buffers appear in blood, intracellular fluid, and extracellular fluid. The main chemical buffers are bicarbonate, phosphate, and protein. The second line of defense against acid-base imbalances is the respiratory system. Chemoreceptors in the brain sense pH changes and vary the rate and depth of respirations to regulate CO2 levels. Alternatively, slower, shallower breathing reduces CO2 excretion, so pH falls. Normal Paco2 is 35 to 45 mm Hg. A higher CO2 level indicates hypoventilation from shallow breathing.
A lower Paco2 level indicates hyperventilation. The respiratory system, which can handle twice as many acids and bases as the buffer systems, responds in minutes, but compensation is temporary. Long-term adjustments require the renal system.
The renal system maintains acid-base balance by absorbing or excreting acids and bases. Also, the kidneys can produce HCO3— to replenish lost supplies.
Unlike the lungs, the kidneys may take 24 hours before starting to restore normal pH. Compensating for imbalances The two disorders of acid-base balance are acidosis and alkalosis. In acidosis, the blood has too much acid or too little base. In alkalosis, the blood has too much base or too little acid. The cause of these acid-base disorders is either respiratory or metabolic.
To regain acid-base balance, the lungs may respond to a metabolic disorder, and the kidneys may respond to a respiratory disorder. If pH remains abnormal, the respiratory or metabolic response is called partial compensation. If the pH returns to normal, the response is called complete compensation.
Keep in mind that the respiratory or renal system will never overcompensate. Respiratory acidosis causes a pH below 7. Blood is normally slightly basic, with a normal pH range of 7.
Usually the body maintains the pH of blood close to 7. A doctor evaluates a person's acid-base balance by measuring the pH and levels of carbon dioxide an acid and bicarbonate a base in the blood.
Overview of Acid-Base Balance
Blood acidity increases when the Level of acidic compounds in the body rises through increased intake or production, or decreased elimination Level of basic alkaline compounds in the body falls through decreased intake or production, or increased elimination Blood alkalinity increases when the level of acid in the body decreases or when the level of base increases. Control of Acid-Base Balance The body's balance between acidity and alkalinity is referred to as acid-base balance.
The blood's acid-base balance is precisely controlled because even a minor deviation from the normal range can severely affect many organs. The body uses different mechanisms to control the blood's acid-base balance. These mechanisms involve the Lungs Buffer systems Role of the lungs One mechanism the body uses to control blood pH involves the release of carbon dioxide from the lungs. Carbon dioxide, which is mildly acidic, is a waste product of the processing metabolism of oxygen and nutrients which all cells need and, as such, is constantly produced by cells.
It then passes from the cells into the blood. The blood carries carbon dioxide to the lungs, where it is exhaled. As carbon dioxide accumulates in the blood, the pH of the blood decreases acidity increases. Entry into the urea cycle is accomplished by the enzyme carbamoyl phosphate synthetase. Metabolic acidosis, acting like a stress response, is associated with an increase in catecholamines and corticosteroids, leading to protein catabolism and the production of increased amounts of ammonia to accompany the low bicarbonate concentrations.
Acidosis decreases hepatic ureagenesis; ammonia is then shunted to form hepatic glutamine rather than urea, a process that spares bicarbonate [ 3 , 11 ].
The increased ammonia produced by the kidney is a result of increased glutamine uptake into proximal tubule cells and acidosis-stimulated renal glutaminase. In this way metabolic acidosis increases glutamine production in liver and increases ammonia produced in kidney.
There is a small shift in urinary nitrogen excretion from urea to ammonia.
Hepatic failure often is associated with acid-base disorders by many mechanisms [ 12 ]: In patients who have acute or chronic pulmonary disease, a common feature is respiratory acidosis or alkalosis. Patients with acute respiratory alkalosis may elevate their pH to greater than 7. In terms of compensation for metabolic disturbances, patients with compromised lung function may have exaggerated hypoventilatory responses to alkalosis and inadequate hyperventilatory responses to acidosis [ 13 ].
Given that there exists a minimal pCO 2 achievable by even the normal lung, compensations for metabolic acidosis are likely to be incomplete in pulmonary disease. That is why severe degrees of metabolic acidosis need to be treated, or ventilator supported, in order to avoid the consequence of abrupt drops in blood pH with any further acidemic insult or tiring of respiratory muscles. The patient with kidney failure less functional mass is more vulnerable to develop acidemia because of a limitation in ammoniagenesis.
Resisting acidifying responses to any imposed metabolic acidosis or respiratory acidosis is impaired in renal failure, since both of those disorders depend on renal ammoniagenesis for compensation.
Renal disease itself will be associated with normal acid-base balance unless the maximum amounts of ammonia necessary to excrete the normally produced acid load are exceeded. That is why patients with low glomerular function, compared to normal, will have a greater tendency to have acidosis with high-protein diets, smaller quantities of bicarbonate-containing diarrhea, or lesser degrees of organic anion acidosis.
If the disease preferentially affects the renal tubules where acid secretion occurs, acidemia will be even more severe. Chronic tubulointerstitial diseases are frequently associated with renal acidosis and hyperkalemia. Patients with acute respiratory acidosis and kidney failure may not have the capacity for renal compensation characteristic of chronic respiratory acidosis if inadequate ammonia is available to enable acid elimination.
Such patients will continue to be severely acidemic and will require adequate bicarbonate replacement to substitute for the expected renal contribution. On the other hand, low levels of glomerular filtration will decrease the amount of bicarbonate filtered. In acidosis this will decrease amounts of bicarbonate lost in the urine; in proximal renal tubular acidosis, the decreased bicarbonate filtration will decrease the severity of, or even cure, the proximal acidosis.
Yet, due to low bicarbonate filtration, an attempt to alkalinize the urine of a nonacidemic patient e. Another observation is that systemic acid-base disturbances are unable to fully compensate [ 14 ]. In theory, full compensation could occur in systemic disease, but almost always, compensation is incomplete Table 1 [ 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 ].
What could be the reason for this phenomenon? In metabolic acidosis, the sympathetic nervous system and corticosteroids are elevated a reason for leukocytosis and hypercatabolic rate. The acid pH and low bicarbonate both stimulate the peripheral chemosensors signaling the medullary center to increase ventilation; the increased ventilatory response results in energy consumption by muscle, including respiratory muscles.
On physical exam, patients with chronic metabolic acidosis are noted to have inspiratory retraction of their intercostal muscles and breathe at high tidal volumes Kussmaul. The work of breathing is increased [ 23 ]. A trade-off exists when compensation is incomplete: An analogy is the classic blue bloater who hypoventilates and pink puffer who hyperventilates in chronic obstructive pulmonary disease: What limits compensation for metabolic acidosis by the kidney is limited capacity for ammoniagenesis, so that despite the adaptive increase in tubular proton secretory mechanisms, new bicarbonate cannot be generated Fig.
The limitation for full compensation of metabolic alkalosis is related to the developed effect of coexisting hypokalemia, volume depletion and hyperaldosteronism which maintain metabolic alkalosis in order to maintain balance of salt, water, and potassium Fig. Only early in vomiting, for example, does the increased filtered bicarbonate reach the urine.
This maintenance represents the limits of compensation: The respiratory compensation for metabolic alkalosis is limited by other stimuli for ventilation. The hypoventilatory response caused by elevated bicarbonate and pH at the level of the peripheral chemosensors is antagonized by hypoxemia which develops with hypoventilation. As a consequence, metabolic alkalosis results in the most variable and incomplete of the compensations.
Compensation in both metabolic acidosis and respiratory acidosis depends on ammoniagenesis that occurs within proximal tubular cells and is limited especially when renal failure develops.
Hypovolemia, hypokalemia, hypochloremia and increased pCO 2 are all essential to maintaining metabolic alkalosis. Renal compensation for respiratory acidosis is enhanced by sodium bicarbonate reabsorption and new bicarbonate generation in the distal nephron and is limited by fluid and electrolyte balance and ammoniagenesis. The decreased glomerular filtration rate due to hypoxemia and hypercarbia and the increased bicarbonate reabsorption caused by high pCO 2 causes extracellular volume expansion as in cor pulmonale.
The elevated plasma bicarbonate level and low chloride reaches a new steady state much like the steady state of mineralocorticoid excess: And since bicarbonate generation depends on ammonia present in the collecting duct lumen, the limited maximal capacity for ammonia synthesis is important.
In this sense, the compensation is maintained by the high pCO 2 and low chloride in analogy to primary hyperaldosteronism where the maintenance of high bicarbonate concentrations is determined by hypokalemia and will correct when potassium is repleted. The chloride depletion is essential to the elevated bicarbonate in compensated respiratory acidosis. In fact, if the pCO 2 is abruptly lowered by mechanical ventilation, a posthypercapnic metabolic alkalosis will develop and persist until adequate chloride is replenished [ 27 ].
Respiratory alkalosis in the chronic phase is somewhat different from all the others. As long as glomerular filtration is not reduced to a great extent, the hypocapnic-driven decreased reabsorption of sodium bicarbonate by the proximal tubule results in bicarbonaturia. This disorder may at times compensate completely to normal pH.
A limitation of bicarbonaturia and therefore full compensation would be low filtration and increased proximal reabsorption from extracellular depletion that could occur as a result of the urinary loss of sodium.
Otherwise the more passive excretion of filtered bicarbonate will stop only when filtered bicarbonate decreases. This is analogous to the way bicarbonaturia stops in the setting of proximal tubular acidosis. The usual diagnostic approach to an acid-base disorder begins with a complete history and physical examination. Clues in the history include: Examples include vomiting metabolic alkalosis , diarrhea metabolic acidosis , chronic obstructive pulmonary disease respiratory acidosis , pneumonia respiratory alkalosis , and so on.
Laboratory tests are usually performed including a basic metabolic profile with electrolytes: The bicarbonate concentration alone does not prove a metabolic disturbance because there are two other variables in equilibrium with bicarbonate: A low plasma bicarbonate is consistent with either metabolic acidosis or respiratory alkalosis. Respiratory alkalosis can be mistaken for renal tubular acidosis if only the plasma bicarbonate is measured.
The level will be low, and the urine pH elevated, in both renal acidosis and respiratory alkalosis; a blood gas analysis of pH will distinguish the two disturbances.
Basics of acid-base balance
When blood gases are drawn and both the pH and bicarbonate are low, there is at least a component of metabolic acidosis and that disorder is the dominant process. However, the finding of a metabolic acidosis does not rule out multiple processes simultaneously present. There are many findings that can be used to diagnose mixed disturbances.
Once the dominant process is identified, it is necessary to assess the degree of compensation by looking at empirical data.
Disorders of Acid-Base Balance: New Perspectives
For example, normal respiratory compensation for metabolic acidosis is predicted based on the expected relationship between bicarbonate and pCO 2 established by empirical observation of subjects with simple metabolic acidosis [ 1 ].
Should the actual pCO 2 be lower than the predicted value, the diagnosis of respiratory alkalosis as second primary disturbance can be made. If the actual pCO 2 is higher than predicted, then a simultaneous respiratory acidosis is present. It is apparent that both metabolic acidosis and its hyperventilatory compensation cause pCO 2 and bicarbonate to fall. The patient with chronic metabolic acidosis who then develops primary hyperventilation may further decrease the bicarbonate concentration while increasing pH.
After the compensatory response to a metabolic acidosis is determined, it is possible to exclude the presence or absence of a primary respiratory disorder, but a mixed metabolic disturbance is still possible. For example, Winter's equation is valid in a mixed metabolic disturbance of metabolic acidosis and alkalosis when the predominant process is acidosis [ 15 ]. In the case where a high chloride acidosis and a low chloride alkalosis coexist, it is not possible to differentiate this double disturbance from a simple metabolic acidosis.
However, it is then useful to determine the serum anion gap. The anion gap is determined by subtracting the sum of chloride and bicarbonate from the serum sodium concentration [ 28 ]. The normal value is approximately mEq per liter corresponding to an amount of charge associated with a normal albumin concentration at normal pH. An elevated anion gap is definitive for a metabolic acidosis Table 2 [ 29 ].
Not only is the presence of an anion gap helpful in the differential diagnosis of the metabolic acidosis, it is also useful in determining the presence of a mixed metabolic disturbance. The calculation of the increment in anion gap is determined as the observed anion gap minus a normal anion gap of 10 mEq per liter. A similar calculation of the decrease in bicarbonate concentration can be made by subtracting the observed bicarbonate concentration from a normal bicarbonate of 25 mEq per liter.
However, if the change in anion gap is greater than the drop in bicarbonate from normal, then there is a process raising the bicarbonate concentration. Such a process is a metabolic alkalosis which may be associated with hypochloremia. An example of this kind of mixed disorder would be a patient who is vomiting and has lactic acidosis or ketoacidosis. In this situation, hypochloremia is frequently observed, suggesting movement of chloride into cells.
The result is hypochloremic, anion gap metabolic acidosis. If the bicarbonate concentration fell more than the anion gap rose, then the second process is most likely a hyperchloremic acidosis Table 3. In the setting of a metabolic acidemia, if the urine contains sodium and potassium with any anion other than chloride, the result will be hyperchloremia [ 30 ].
If the urinary anion is bicarbonate, then the hyperchloremic acidosis that results is known as a renal tubular acidosis. If the excreted anion is not bicarbonate, for example ketoacid or lactate anion, then the appearance in the blood will also be that of a hyperchloremic acidosis.
In the extreme, where all the organic anion is excreted with sodium and potassium in the urine, the appearance in the blood will be that of a nonanion gap hyperchloremic metabolic acidosis. Some patients with ketoacidosis or glue-sniffing acidosis due to hippurate derived from toluene, who have a high glomerular filtration rate, can present with a hyperchloremic acidosis; rather than having a blood anion gap, the urine demonstrates the charge gap.
In that way, a gap acidosis may be misdiagnosed as a renal tubular acidosis. In other words, what is the fate of those hydrogen ions as pH changes from normal? Thus, it is problematic to choose a single buffer system to explain acid-base phenomena.
Yet, the isohydric principle is the basis of the traditional approach using bicarbonate and pCO 2 to understand acid-base balance [ 31 ]. In the above equation, 0. The isohydric principle states that the hydrogen ion concentration is equal to the ratio of acid to base multiplied by the dissociation constant for each buffer pair in the body that can pick up a proton.
This includes phosphate, albumin, hemoglobin and a host of other proteins. This becomes a nonlinear relationship for bicarbonate since the ratio for each buffer pair is different for differing pH, a fact central to the definition of pK. This weakness is illustrated by the equation below, used clinically to determine replacement amounts of bicarbonate for an acidemic patient to normalize the bicarbonate concentration:. In this equation, it would appear that the bicarbonate volume of distribution is 0.
However, a more likely estimate of bicarbonate's volume of distribution is closer to the extracellular volume, or 0. In the above equation, the 0. This equation is used to estimate the bicarbonate deficit or excess and therefore is used as a guide to replacement of bicarbonate in acidosis or HCl in alkalosis.
However, the percent contribution of bicarbonate is not always the 0. It falls as bicarbonate goes down in acidosis and rises as bicarbonate goes up in alkalosis. Furthermore, one would not likely consider bicarbonate replacement in a patient with a pH of 7. What this means is that due to the nonlinearity of the isohydric principle, the apparent volume of distribution for bicarbonate increases with acidosis and decreases with alkalosis due to the relative importance of bicarbonate versus phosphates and other proteins as pH changes.
Clinically, the apparent volume of distribution could exceed body weight if calculated in acidosis since more bicarbonate than expected would need to be given to correct severe acidosis.
Despite these shortcomings, the calculation can be successfully used if only a fraction of the calculated amount is given and re-calculations are frequent. Of greatest danger is using this equation to calculate an amount of HCl to give an alkalemic patient to lower the serum bicarbonate.
Since the apparent volume of distribution is much less than would be calculated from this equation, the chances of overtreating with acid are great. Another consequence of the isohydric principle is that in vomiting-induced losses of hydrochloric acid, the amount of hydrogen ion that is lost is equal to the chloride that is lost, not to the amount of bicarbonate that is gained in the extracellular fluid.
In other words, because there is a high blood pH, the bicarbonate distribution will be smaller than predicted by the 0. Since the buffer capacity of bicarbonate is greater than predicted for pH of 7. The traditional approach often considers acid-base and electrolyte disorders separately, whereas in clinical practice the disturbances are interconnected.
Take acute versus chronic respiratory acidosis as example: That is because there is no room electrically speaking, in the extracellular fluid for additional bicarbonate anion needed to compensate. That would require a decrease in another anion or a rise in cation for electroneutrality purposes.
Only after the renal excretion of the anion chloride in the urine does the serum bicarbonate concentration rise. This could be viewed as a time-dependent increase in ammoniagenesis and ammonium chloride excretion which then allows for bicarbonate concentration to be maintained at a higher level. In other words, it is the hypochloremia that allows maintenance of electroneutrality, and increases in plasma bicarbonate concentration as acute respiratory acidosis transitions to chronic respiratory acidosis.
Two interpretations of this phenomena are either that the compensation is primarily due to an increase in renal bicarbonate generation versus the excretion of chloride to maintain electroneutrality [ 33 , 34 , 35 , 36 , 37 , 38 ]. In both cases, the importance of ammonium in the urine is significant.
Most acid-base disorders develop in the context of either gains of fluid and electrolytes or losses of fluid and electrolytes from the body. To begin our discussion, let us only consider strong ions that are completely dissociated in body fluids.
For the moment, we will not consider the hydrogen and bicarbonate ion concentrations. If the normal extracellular sodium concentration is m M and chloride concentration is m M , then a gain or loss of fluid with precisely those same concentrations should have no effect on acid-base balance.
For example, if the loss from the extracellular fluid compartment contained relatively more chloride than sodium, then the change observed for electrolytes in the extracellular fluid would be hypochloremia. If the loss contained relatively less chloride than sodium compared to the normal extracellular fluid content, then the result would be hyperchloremia.
The same consequences on the extracellular fluid sodium and chloride concentrations would occur if the gains of fluid containing sodium and chloride were disproportionate to normal extracellular fluid values. For example, if isotonic sodium chloride were infused into a patient, there would be a tendency for hyperchloremia to develop because the 1:Aldosterone also increases intercalated cell proton secretion resulting in further bicarbonate reabsorption.
Key Messages: Cushing syndrome and ectopic secretion of ACTH are other considerations.
Considering sodium, potassium and chloride in the urine, the excretion of sodium and potassium concentrations relative to chloride that are disproportionate to that which exists in the extracellular fluid can predict whether the loss of that urine will have an acidifying or alkalinizing effect on the extracellular fluid. As long as glomerular filtration is not reduced to a great extent, the hypocapnic-driven decreased reabsorption of sodium bicarbonate by the proximal tubule results in bicarbonaturia.
Although it is customary to assess acid-base disorders by its reflection in the extracellular fluid rather than the intracellular space, such practice is an oversimplification and also a potential source of error, since so many pH-dependent metabolic processes and functions relate to intracellular electrolytes and acid-base.
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