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What Is The Value For Metabolic Acidosis?

Abg Interpreter

Abg Interpreter

pH CO2 HCO3 Result appears in here. Normal Arterial Blood Gas Values pH 7.35-7.45 PaCO2 35-45 mm Hg PaO2 80-95 mm Hg HCO3 22-26 mEq/L O2 Saturation 95-99% BE +/- 1 Four-Step Guide to ABG Analysis Is the pH normal, acidotic or alkalotic? Are the pCO2 or HCO3 abnormal? Which one appears to influence the pH? If both the pCO2 and HCO3 are abnormal, the one which deviates most from the norm is most likely causing an abnormal pH. Check the pO2. Is the patient hypoxic? I used Swearingen's handbook (1990) to base the results of this calculator. The book makes the distinction between acute and chronic disorders based on symptoms from identical ABGs. This calculator only differentiates between acute (pH abnormal) and compensated (pH normal). Compensation can be seen when both the PCO2 and HCO3 rise or fall together to maintain a normal pH. Part compensation occurs when the PCO2 and HCO3 rise or fall together but the pH remains abnormal. This indicates a compensatory mechanism attempted to restore a normal pH. I have not put exact limits into the calculator. For example, it will perceive respiratory acidosis as any pH < 7.35 and any CO2 > 45 (i.e. a pH of 1 and CO2 of 1000). These results do not naturally occur. pH PaCO2 HCO3 Respiratory Acidosis Acute < 7.35 > 45 Normal Partly Compensated < 7.35 > 45 > 26 Compensated Normal > 45 > 26 Respiratory Alkalosis Acute > 7.45 < 35 Normal Partly Compensated > 7.45 < 35 < 22 Compensated Normal < 35 < 22 Metabolic Acidosis Acute < 7.35 Normal < 22 Partly Compensated < 7.35 < 35 < 22 Compensated Normal < 35 < 22 Metabolic Alkalosis Acute > 7.45 Normal > 26 Partly Compensated > 7.45 > 45 > 26 Compensated Normal > 45 > 26 Mixed Disorders It's possible to have more than one disorder influencing blood gas values. For example ABG's with an alkale Continue reading >>

Feline Chronic Kidney Disease

Feline Chronic Kidney Disease

Home > Key Issues > Metabolic Acidosis Overview Metabolic acidosis means that the levels of acid in the cat's body are too high. It is extremely common in CKD cats, usually cats in Stage IV, and can make the cat feel ill and the CKD progress faster. It can be tricky to diagnose, but fortunately it is relatively easy to treat. What is Metabolic Acidosis? There is a delicate balance within the body known as acid-base balance (pH): Metabolic acidosis means that this balance is disrupted, in that levels of acid in the cat's body are too high, so the blood pH is too low (acidic). Acid is produced in the body as a result of diet. In healthy cats, the kidneys help to balance acid levels in the body in two ways: Bicarbonate ions (which are alkaline) in the kidneys help protect against acid build-up in the body; Any excess acids that do arise are flushed from the body by the kidneys. Unfortunately the excessive urine flow of CKD washes the protective bicarbonate ions out of the kidneys. On the other hand, the damaged kidneys may no longer flush the acids from the body properly. As a result of these damaged mechanisms, acidity levels in the blood rise, and the body’s pH becomes too low. This is known as acidosis. "Metabolic" means that the acidosis is caused by kidney disease. This is to differentiate it from another type of acidosis known as respiratory acidosis, which is caused by the lungs not expelling carbon dioxide properly. I know a lot of people get confused by the word "acidosis" and think it is the same thing as excess stomach acid, but that is not the case. Gastrin is a gastrointestinal hormone which stimulates the secretion of gastric acid, which helps the stomach digest food. The kidneys are responsible for the excretion of gastrin, but in CKD this function may not Continue reading >>

Metabolic Acidosis Workup

Metabolic Acidosis Workup

Approach Considerations Often the first clue to metabolic acidosis is a decreased serum HCO3- concentration observed when serum electrolytes are measured. Remember, however, that a decreased serum [HCO3-] level can be observed as a compensatory response to respiratory alkalosis. An [HCO3-] level of less than 15 mEq/L, however, almost always is due, at least in part, to metabolic acidosis. The only definitive way to diagnose metabolic acidosis is by simultaneous measurement of serum electrolytes and arterial blood gases (ABGs), which shows pH and PaCO2 to be low; calculated HCO3- also is low. (For more information, see Metabolic Alkalosis.) A low serum HCO3- and a pH of less than 7.40 upon ABG analysis confirm metabolic acidosis. Go to Pediatric Metabolic Acidosis and Emergent Management of Metabolic Acidosis for complete information on these topics. Continue reading >>

What Is Metabolic Acidosis?

What Is Metabolic Acidosis?

Metabolic acidosis happens when the chemical balance of acids and bases in your blood gets thrown off. Your body: Is making too much acid Isn't getting rid of enough acid Doesn't have enough base to offset a normal amount of acid When any of these happen, chemical reactions and processes in your body don't work right. Although severe episodes can be life-threatening, sometimes metabolic acidosis is a mild condition. You can treat it, but how depends on what's causing it. Causes of Metabolic Acidosis Different things can set up an acid-base imbalance in your blood. Ketoacidosis. When you have diabetes and don't get enough insulin and get dehydrated, your body burns fat instead of carbs as fuel, and that makes ketones. Lots of ketones in your blood turn it acidic. People who drink a lot of alcohol for a long time and don't eat enough also build up ketones. It can happen when you aren't eating at all, too. Lactic acidosis. The cells in your body make lactic acid when they don't have a lot of oxygen to use. This acid can build up, too. It might happen when you're exercising intensely. Big drops in blood pressure, heart failure, cardiac arrest, and an overwhelming infection can also cause it. Renal tubular acidosis. Healthy kidneys take acids out of your blood and get rid of them in your pee. Kidney diseases as well as some immune system and genetic disorders can damage kidneys so they leave too much acid in your blood. Hyperchloremic acidosis. Severe diarrhea, laxative abuse, and kidney problems can cause lower levels of bicarbonate, the base that helps neutralize acids in blood. Respiratory acidosis also results in blood that's too acidic. But it starts in a different way, when your body has too much carbon dioxide because of a problem with your lungs. Continue reading >>

What Chemical Processes Or Reactions Contribute To Metabolic Acidosis?

What Chemical Processes Or Reactions Contribute To Metabolic Acidosis?

There are three primary states metabolic acidosis. Their underlying physiological causes are from diabetes (ketoacidosis), normal anion gap acidosis from ailments such as kidney malfunction (renal tubular acidosis or more specifically hyperchloremic acidosis), and rare congenital mitochondrial disorders (lactic acidosis). More common causes of metabolic acidosis may come from liver disease or damage or from the ingestion of certain anti-retroviral drugs and poisons such as arsenic. In ketoacidosis, the body does not have enough insulin which allows glucose to be transported across the cell membranes. The body's response is to try to compensate for the supposed lack of energy source (starvation defense, even though there is plenty in the blood) by digesting fat which is converted by the liver into alternative energy sources, i.e. ketones such as acetoacetate and the carboxylic acid β-hydroxybutyrate. These byproducts are acidic and lower the pH of the blood. In renal tubular acidosis (RTA) the kidneys are not acidifying the urine as efficiently as they should which allows acid in the blood to accumulate. RTA is a normal anion gap acidosis during which the alpha intercalated cells fail to secret acid. This can be caused by toxin damage from toluene or lithium carbonate among others, or by mutations. Two well known genetic causes of RTA are a mutation in the anion exchanger AE1 (Band 3) transport protein that controls chloride and bicarbonate exchange across the plasma membrane, and mutations to the apical proton pump vH+-ATPase. A reduction in plasma bicarb concentration and increased chloride prevents pH buffering and reduces the pH. Lesser known mutations that have the same effect are in the family of serine-threonine protein kinases WNK1 or WNK4, specifically, the min Continue reading >>

Metabolic Acidosis In Emergency Medicine Workup

Metabolic Acidosis In Emergency Medicine Workup

Laboratory Studies Arterial blood gas analysis A low HCO3 level found on an automated sequential multiple analyzer (SMA) (eg, serum chemistries) is often the first clue to the presence of a metabolic acidosis; however, it cannot be the only consideration in the diagnosis of metabolic acidosis. A low HCO3 level can be caused by metabolic acidosis, a metabolic compensation of a respiratory alkalosis, or a laboratory error. The HCO3 level that is calculated by the arterial blood gas (ABG) machine, which uses the Henderson-Hasselbalch equation, represents a more accurate measure of the plasma HCO3 level than the SMA measurement. It is suggested that the HCO3 level that is determined from the ABG be used in the anion gap calculation instead of the HCO3 level found using the SMA. Measurement of pH and PCO2 by ABG in a patient with a low HCO3 level makes it possible to differentiate a metabolic compensation of a respiratory alkalosis from a primary metabolic acidosis. Measurement of PCO2 also makes it possible to judge the appropriateness of respiratory compensation of a metabolic acidosis, and to detect respiratory acidosis, which is signified by an elevated PCO2 level. Oxygenation does not affect the acid-base status of a patient and generally should not be part of the discussion unless severe hypoxia is leading to ischemia. In that case, measurement of PO2 can identify severe hypoxia as a precipitant of lactic acidosis. ABGs also measure base excess/base deficit (BE/BD), which is the best indicator of the degree of acidosis/alkalosis. BE/BD is measured by gauging the amount of acid or base that is required to titrate the patient's blood sample to a pH of 7.40, given a PCO2 level of 40 mm Hg at 37 degrees Celsius. BE/BD is a more accurate reflection of the body's state, and Continue reading >>

A Primer On Arterial Blood Gas Analysis By Andrew M. Luks, Md(cont.)

A Primer On Arterial Blood Gas Analysis By Andrew M. Luks, Md(cont.)

Step 4: Identify the compensatory process (if one is present) In general, the primary process is followed by a compensatory process, as the body attempts to bring the pH back towards the normal range. If the patient has a primary respiratory acidosis (high PCO2 ) leading to acidemia: the compensatory process is a metabolic alkalosis (rise in the serum bicarbonate). If the patient has a primary respiratory alkalosis (low PCO2 ) leading to alkalemia: the compensatory process is a metabolic acidosis (decrease in the serum bicarbonate) If the patient has a primary metabolic acidosis (low bicarbonate) leading acidemia, the compensatory process is a respiratory alkalosis (low PCO2 ). If the patient has a primary metabolic alkalosis (high bicarbonate) leading to alkalemia, the compensatory process is a respiratory acidosis (high PCO2 ) The compensatory processes are summarized in Figure 2. (opens in a new window) Important Points Regarding Compensatory Processes There are several important points to be aware of regarding these compensatory processes: The body never overcompensates for the primary process. For example, if the patient develops acidemia due to a respiratory acidosis and then subsequently develops a compensatory metabolic alkalosis (a good example of this is the COPD patient with chronic carbon dioxide retention), the pH will move back towards the normal value of 7.4 but will not go to the alkalemic side of normal This might result in a pH of 7.36, for example but should not result in a pH such as 7.44 or another value on the alkalemic side of normal. If the pH appears to "over-compensate" then an additional process is at work and you will have to try and identify it. This can happen with mixed acid-base disorders, which are described further below. The pace of co Continue reading >>

Serum Anion Gap: Its Uses And Limitations In Clinical Medicine

Serum Anion Gap: Its Uses And Limitations In Clinical Medicine

Abstract The serum anion gap, calculated from the electrolytes measured in the chemical laboratory, is defined as the sum of serum chloride and bicarbonate concentrations subtracted from the serum sodium concentration. This entity is used in the detection and analysis of acid-base disorders, assessment of quality control in the chemical laboratory, and detection of such disorders as multiple myeloma, bromide intoxication, and lithium intoxication. The normal value can vary widely, reflecting both differences in the methods that are used to measure its constituents and substantial interindividual variability. Low values most commonly indicate laboratory error or hypoalbuminemia but can denote the presence of a paraproteinemia or intoxication with lithium, bromide, or iodide. Elevated values most commonly indicate metabolic acidosis but can reflect laboratory error, metabolic alkalosis, hyperphosphatemia, or paraproteinemia. Metabolic acidosis can be divided into high anion and normal anion gap varieties, which can be present alone or concurrently. A presumed 1:1 stoichiometry between change in the serum anion gap (ΔAG) and change in the serum bicarbonate concentration (ΔHCO3−) has been used to uncover the concurrence of mixed metabolic acid-base disorders in patients with high anion gap acidosis. However, recent studies indicate variability in the ΔAG/ΔHCO3− in this disorder. This observation undercuts the ability to use this ratio alone to detect complex acid-base disorders, thus emphasizing the need to consider additional information to obtain the appropriate diagnosis. Despite these caveats, calculation of the serum anion gap remains an inexpensive and effective tool that aids detection of various acid-base disorders, hematologic malignancies, and intoxication Continue reading >>

Simple Method Of Acid Base Balance Interpretation

Simple Method Of Acid Base Balance Interpretation

A FOUR STEP METHOD FOR INTERPRETATION OF ABGS Usefulness This method is simple, easy and can be used for the majority of ABGs. It only addresses acid-base balance and considers just 3 values. pH, PaCO2 HCO3- Step 1. Use pH to determine Acidosis or Alkalosis. ph < 7.35 7.35-7.45 > 7.45 Acidosis Normal or Compensated Alkalosis Step 2. Use PaCO2 to determine respiratory effect. PaCO2 < 35 35 -45 > 45 Tends toward alkalosis Causes high pH Neutralizes low pH Normal or Compensated Tends toward acidosis Causes low pH Neutralizes high pH Step 3. Assume metabolic cause when respiratory is ruled out. You'll be right most of the time if you remember this simple table: High pH Low pH Alkalosis Acidosis High PaCO2 Low PaCO2 High PaCO2 Low PaCO2 Metabolic Respiratory Respiratory Metabolic If PaCO2 is abnormal and pH is normal, it indicates compensation. pH > 7.4 would be a compensated alkalosis. pH < 7.4 would be a compensated acidosis. These steps will make more sense if we apply them to actual ABG values. Click here to interpret some ABG values using these steps. You may want to refer back to these steps (click on "linked" steps or use "BACK" button on your browser) or print out this page for reference. Step 4. Use HC03 to verify metabolic effect Normal HCO3- is 22-26 Please note: Remember, the first three steps apply to the majority of cases, but do not take into account: the possibility of complete compensation, but those cases are usually less serious, and instances of combined respiratory and metabolic imbalance, but those cases are pretty rare. "Combined" disturbance means HCO3- alters the pH in the same direction as the PaCO2. High PaCO2 and low HCO3- (acidosis) or Low PaCO2 and high HCO3- (alkalosis). Continue reading >>

Evaluation Of Metabolic Acidosis

Evaluation Of Metabolic Acidosis

Diagnostic Approach A systematic evaluation of acid-base status of the patient provides insight into the underlying medical problem. The differential diagnosis of these disorders can be narrowed down with the help of the patient's clinical information and some laboratory data. These clinical conditions with acid-base disorders can be effectively evaluated by a stepwise pathophysiologic approach. [2] [3] ABG analysis and a comprehensive metabolic panel (CMP) should be requested. The laboratory data required to approach a suspected acid-base disorder are obtained from the ABG, which provides information about pH, PaO2, PaCO2, and calculated HCO3 values, and venous serum CMP, which provides Na+, K+, Cl, and total CO2 content (TCO2). TCO2 represents total carbon dioxide concentration in the serum including dissolved CO2, bicarbonate, carbonate, and carbonic acid. Dissolved CO2 is a small fraction of TCO2. TCO2 on the serum electrolyte panel mainly represents the plasma bicarbonate concentration. The following steps are required to interpret the data and determine the cause of metabolic acidosis 1. Determine the disturbance in pH Arterial pH indicates the ongoing disturbance - acidosis versus alkalosis. At sea level the normal pH is 7.42 ± 0.02, with a range of 7.35 to 7.45. Decrease in arterial pH <7.35 suggests that the major ongoing disturbance is acidosis. 2. Identify the primary disorder To determine the primary disorder, the directional changes of serum HCO3 and arterial PaCO2 from the normal and their relation with change in arterial pH are examined. If the pH is low and HCO3 is low, then the primary disorder is metabolic acidosis. 3. Assess compensation in response to the primary disorder With simple metabolic acidosis, the normal adaptive respiratory response will Continue reading >>

Acid-base (anesthesia Text)

Acid-base (anesthesia Text)

There are four native buffer systems – bicarbonate, hemoglobin, protein, and phosphate systems. Bicarbonate has a pKa of 6.1, which is not ideal. Hemoglobin has histidine residues with a pKa of 6.8. Chemoreceptors in the carotid bodies, aortic arch, and ventral medulla respond to changes in pH/pCO2 in a matter of minutes. The renal response takes much longer. Arterial vs. Venous Gases Venous blood from the dorsum of the hand is moderately arterialized by general anesthesia, and can be used as a substitute for an ABG. pCO2 will only be off by ~ 5 mm Hg, and pH by 0.03 or 0.04 units [Williamson et. al. Anesth Analg 61: 950, 1982]. Confounding variables include air bubbles, heparin (which is acidic), and leukocytes (aka “leukocyte larceny”). VGB/ABG samples should be cooled to minimize leukocyte activity, however when blood is cooled, CO2 solubility increases (less volatile), and thus pCO2 drops. As an example – a sample taken at 37°C and at 7.4 will actually read as a pH of 7.6 if measured at 25°C. Most VBG/ABGs are actually measured at 37°C. A-aDO2 increases with age, as well as with increased FiO2 and vasodilators (which impair hypoxic pulmonary vasoconstriction). In the setting of a shunt, pulse oximetry can be misleading, thus the A-aDO2 should be calculated. If PaO2 is > 150 mm Hg (i.e., Hg saturation is essentially 100%), every 20 mm Hg of A-aDO2 represents 1% shunting of cardiac output. A/a is even better than A-aDO2 because it is independent of FiO2. PaO2/FiO2 is a reasonable alternative, with hypoxia defined as PaO2/FiO2 < 300 (a PaO2/FiO2 < 200 suggests a shunt fraction of 20% or more). Mixed venous blood should have a pO2 of ~ 40 mm Hg. Values < 30 mm Hg suggest hypoxemia, although one must always keep in mind that peripheral shunting and cyanide tox Continue reading >>

Normal And Abnormal Value Ranges And Their Interpretations As Used On The Acidbase.org Website

Normal And Abnormal Value Ranges And Their Interpretations As Used On The Acidbase.org Website

value to be calculated units very low values moderately low values slightly low values therapeutic or normal range slightly high values moderately high values very high values pH < 7.1 severe acidosis 7.1 <==> 7.25 moderate acidosis 7.25 <==> 7.35 slight acidosis 7.35 -- 7.45 7.45 <==> 7.5 slight alkalosis 7.5 <==> 7.6 moderate alkalosis > 7.6 severe alkalosis lactate mmol/l up to 2.2 2.2 <==> 3 slight lactic acid metabolic acidosis 3 <==> 7 moderate lactic acid metabolic acidosis > 7 severe lactic acid metabolic acidosis albumin the most prominent of the weak acids read more! g/l < 15 severe hypalbuminaemia - metabolic alkalosis 15 <==> 28 moderate hypalbuminaemia - metabolic alkalosis 28 <==> 38 slight hypalbuminaemia - minimal metabolic alkalosis 38 -- 45 45 <==> 60 slight hyperalbuminaemia - metabolic acidosis 60 <==> 70 moderate hyperalbuminaemia - metabolic acidosis > 70 severe hyperalbuminaemia - metabolic acidosis PCO2 kPa < 2.5 severe respiratory alkalosis 2.5 <==> 3.5 moderate respiratory alkalosis 3.5 <==> 4.7 slight respiratory alkalosis 4.7 -- 5.9 5.9 <==> 7 slight respiratory acidosis 7 <==> 8.9 moderate respiratory acidosis > 8.9 severe respiratory acidosis phosphate mmol/l < 0.5 a very low value for phosphate! - this has a small alkalinising effect 0.5 <==> 0.75 a low value for phosphate - this has a slightly alkalinising effect 0.75 -- 1.4 1.4 <==> 1.9 a slightly high value for phosphate - this has a small acidifying effect > 1.9 a high value for phosphate - this has an acidifying effect HCO3 mEq/l < 19 19 <==> 22 22 -- 26 26 <==> 29 > 29 BE (calculated according to the van Slyke formula) read more! mEq/l < -4 -4 <==> -2 -2 -- +2 +2 <==> +4 > +4 Na- Cl correction your Na and/or Cl values differ considerably from the normal ranges on our website - anion Continue reading >>

Respiratory Compensation

Respiratory Compensation

Metabolic Acidosis Respiratory compensation for metabolic disorders is quite fast (within minutes) and reaches maximal values within 24 hours. A decrease in Pco2 of 1 to 1.5 mm Hg should be observed for each mEq/L decrease of in metabolic acidosis.27 A simple rule for deciding whether the fall in Pco2 is appropriate for the degree of metabolic acidosis is that the Pco2 should be equal to the last two digits of the pH. For example, compensation is adequate if the Pco2 decreases to 28 when the pH is 7.28. Alternatively, the Pco2 can be predicted by adding 15 to the observed (down to a value of 12). Although reduction in Pco2 plays an important role in correcting any metabolic acidosis, evidence suggests that it may in some respects be counterproductive because it inhibits renal acid excretion. Fetoplacental Elimination of Metabolic Acid Load Fetal respiratory and renal compensation in response to changes in fetal pH is limited by the level of maturity and the surrounding maternal environment. However, although the placentomaternal unit performs most compensatory functions,3 the fetal kidneys have some, although limited, ability to contribute to the maintenance of fetal acid–base balance. The most frequent cause of fetal metabolic acidosis is fetal hypoxemia owing to abnormalities of uteroplacental function or blood flow (or both). Primary maternal hypoxemia or maternal metabolic acidosis secondary to maternal diabetes mellitus, sepsis, or renal tubular abnormalities is an unusual cause of fetal metabolic acidosis. Pregnant women, at least in late gestation, maintain a somewhat more alkaline plasma environment compared with that of nonpregnant control participants. This pattern of acid–base regulation in pregnant women is present during both resting and after maximal e Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is primary reduction in bicarbonate (HCO3−), typically with compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly subnormal. Metabolic acidoses are categorized as high or normal anion gap based on the presence or absence of unmeasured anions in serum. Causes include accumulation of ketones and lactic acid, renal failure, and drug or toxin ingestion (high anion gap) and GI or renal HCO3− loss (normal anion gap). Symptoms and signs in severe cases include nausea and vomiting, lethargy, and hyperpnea. Diagnosis is clinical and with ABG and serum electrolyte measurement. The cause is treated; IV sodium bicarbonate may be indicated when pH is very low. Acidemia (arterial pH < 7.35) results when acid load overwhelms respiratory compensation. Causes are classified by their effect on the anion gap (see The Anion Gap and see Table: Causes of Metabolic Acidosis). High anion gap acidosis Ketoacidosis is a common complication of type 1 diabetes mellitus (see diabetic ketoacidosis), but it also occurs with chronic alcoholism (see alcoholic ketoacidosis), undernutrition, and, to a lesser degree, fasting. In these conditions, the body converts from glucose to free fatty acid (FFA) metabolism; FFAs are converted by the liver into ketoacids, acetoacetic acid, and beta-hydroxybutyrate (all unmeasured anions). Ketoacidosis is also a rare manifestation of congenital isovaleric and methylmalonic acidemia. Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Lactate accumulation results from a combination of excess formation and decreased utilization of lactate. Excess lactate production occurs during states of anaerobic metabolism. The most serious form occurs during the various types o Continue reading >>

Differential Diagnosis Of Nongap Metabolic Acidosis: Value Of A Systematic Approach

Differential Diagnosis Of Nongap Metabolic Acidosis: Value Of A Systematic Approach

Go to: Recognition and Pathogenesis of the Hyperchloremia and Hypobicarbonatemia of Nongap Acidosis A nongap metabolic acidosis is characterized by a serum anion gap that is unchanged from baseline, or a decrease in serum [HCO3−] that exceeds the rise in the anion gap (5,6). Whenever possible, the baseline anion gap of the patient should be used rather than the average normal value specific to a particular clinical laboratory (6) and the anion gap should be corrected for the effect of a change in serum albumin concentration (7). These steps will reduce the chance that a co-existing high anion gap acidosis will be missed if the increase in the serum anion gap does not cause the value to exceed the upper limit of the normal range (8,9). Nongap metabolic acidosis (hyperchloremic) refers a metabolic acidosis in which the fall in serum [HCO3−] is matched by an equivalent increment in serum Cl− (6,10). The serum anion gap might actually decrease slightly, because the negative charges on albumin are titrated by accumulating protons (6,11). Hyperchloremic acidosis is a descriptive term, and does not imply any primary role of chloride in the pathogenesis of the metabolic acidosis. As shown in Figure 1, a nongap metabolic acidosis can result from the direct loss of sodium bicarbonate from the gastrointestinal tract or the kidney, addition of hydrochloric acid (HCl) or substances that are metabolized to HCl, impairment of net acid excretion, marked urinary excretion of organic acid anions with replacement with endogenous or administered Cl− (12,13), or administration of Cl−-rich solutions during resuscitation (14). The development of hyperchloremic acidosis from administration of HCl is easy to visualize, with titrated HCO3− being replaced by Cl−. Similarly, gastroin Continue reading >>

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