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# Metabolic Acidosis Compensation Formula

## How To Compute Expected Pco2 In Chronic Metabolic Acidosis ?

How to compute PaCO2 during chronic metabolic acidosis? We dont have to compute for chronic metabolic acidosis (CMA) since the PaCO2 value in mmHg is equal to the two digits of the pH value For instance IF pH = 7.25, PaCO2 should be about 25 mmHg, With this formula, we can immediately focus on the respiratory compensation: If PaCO2 is significantly greater than 25 mmHg, the respiratory compensation is inadequate, thus a respiratory insufficiency is associated; If PaCO2 is largely lower than 25 mmHg, the respiratory is higher than CMA required, therefore a respiratory alkalosis is associated to CMA. Furthermore, according to the alveolar gas equation (Fi02 of 21%): Pa02 + PaCO2= 140 mmHg; in this case, in absence of pulmonary disease, PaO2 should be elevated, near 115 mmHg FG Brivet, FM Jacobs: Anomalies de lEquilibre Acido-basique dOrigine Mtabolique in Ranimation Mdicale ; Collge National des Enseignants de Ranimation Mdicale, Masson Paris 2009 PP 1356-1365. In the same way for ACUTE Metabolic Acidosis, instead of using Narinss formula: It is easier to use Schlichtigs formula: Delta PaCO2 (mmHg) = Standard base excess (2) Thus in case of acute metabolic acidosis, with the same value of pH (7.25) and an SBE of 18, for instance (SBE value being systematically reported by lab but rarely used.), PaC02 should be near 22 mmHg (40- 18). If PaCO2 value is greater than the expected value, respiratory compensation is inadequate, the patient is at risk of respiratory failure, whereas if PaCO2 is lower than 18 we can claim that a respiratory alkalosis is associated. With this approach I can say goodbye Mr. Davenport, you are too sophisticated for me at 5 in the morning 1/ Narins RG, Emmet M. Simple and mixed acid-base disorders: a practical approach. Medicine, 1980, 59: 161-167. Continue reading >>

## Response To Disturbances

The body tries to minimize pH changes and responds to acid-base disturbances with body buffers, compensatory responses by the lungs and kidney (to metabolic and respiratory disturbances, respectively) and by the kidney correcting metabolic disturbances. Body buffers: There are intracellular and extracellular buffers for primary respiratory and metabolic acid-base disturbances. Intracellular buffers include hemoglobin in erythrocytes and phosphates in all cells. Extracellular buffers are carbonate (HCO3–) and non-carbonate (e.g. protein, bone) buffers. These immediately buffer the rise or fall in H+. Compensation: This involves responses by the respiratory tract and kidney to primary metabolic and respiratory acid-base disturbances, respectively. Compensation opposes the primary disturbance, although the laboratory changes in the compensatory response parallel those in the primary response. This concept is illustrated in the summary below. Respiratory compensation for a primary metabolic disturbance: Alterations in alveolar ventilation occurs in response to primary metabolic acid-base disturbances. This begins within minutes to hours of an acute primary metabolic disturbance. Note that complete compensation via this mechanism may take up to 24 hours. Renal compensation for a primary respiratory disturbance: Here, the kidney alters excretion of acid (which influences bases as well) in response to primary respiratory disturbances. This begins within hours of an acute respiratory disturbance, but take several days (3-5 days) to take full effect. Correction of acid-base changes: Correction of a primary respiratory acid-base abnormality usually requires medical or surgical intervention of the primary problem causing the acid-base disturbance, e.g. surgical relief of a colla Continue reading >>

## Metabolic Acidosis - An Overview | Sciencedirect Topics

Metabolic acidosis is a process that leads to the accumulation of H+ ions and the decrease in the content of HCO3 ions in the body. Larry R. Engelking, in Textbook of Veterinary Physiological Chemistry (Third Edition) , 2015 Metabolic acidosis is the most common acid-base disorder recognized in domestic animals. Like in respiratory alkalosis (see Chapter 91), the bicarbonate buffer equation is shifted to the left in metabolic acidosis (Fig. 87-1). Also, with an excess acid load or decreased urinary acid excretion, either an increased or normal plasma AG can be seen (see Table 86-1). What determines whether the AG will increase in metabolic acidosis? Whenever H+ is added to the system, HCO3 is consumed. The hydrogen cation cannot be added without an anion. Therefore, for each HCO3 consumed, a negative charge of some other type (which accompanied the H+) is added to body fluids. If the anion happens to be Cl, no change in the AG will develop. However, if it is any other anion, the AG will be increased. Kamel S. Kamel MD, FRCPC, Mitchell L. Halperin MD, FRCPC, in Fluid, Electrolyte and Acid-Base Physiology (Fifth Edition) , 2017 What is the cause of the metabolic acidosis in this patient? Metabolic acidosis in this patient was not simply the result of loss of NaHCO3 in diarrheal fluid because the PAnion gap was 26 mEq/L. L-Lactic acidosis is unlikely because there was no hemodynamic problem, liver function tests were normal, and the time period was too short for a nutritional deficiency (e.g., thiamin and/or riboflavin deficiency) that may have caused L-lactic acidosis. Moreover, he did not ingest drugs that may be associated with L-lactic acidosis. There was no history of diabetes mellitus or the intake of ethanol, and his blood sugar was normal. Later, L-lactic acidosis Continue reading >>

## Acid Base Calculation Made Easy !

Posted by Ash from IP 74.138.144.66 on October 12, 2006 at 17:50:13: 6 steps to ABG analysis, go step by step in the very same order:- 1.Chk whether the pt is academic or alkalemic,by looking at the arterial pH (NL = 7.38 7.42) 2. Chk whether the ABG abnormality is due to a primary repiratory or metabolic disorder by chking the PCo2 levels( NL 38-42) and HCO3 levels (NL 22-26) 3. Now if there is respiratory component identified,chk whether this is acute or chronic respiratory acidosis or alkalosis. 4. Now if u identify a metabolic component ,chk whether it is high anion or normal anion gap M.Acidosis 5. Chk wether the respiratory system is adequetly compensating for this primary metabolic disorder. 6. Now u identify a high anion gap M.A,chk the corrected HCO3 level,y we do this coz to know wether there was a intial primary disorder ,before this new metabolic disorder developed. VERY IMPO FORMULAS :- U have to learn the formulas byheart) In Metabolic acidosis pH and HCO3 (DECREASES) So to compensate for every 1 mmol/l of drop in HCO3 , 1.2mmhg of PCO2 shld decrease So to compensate for every 1 mmol/l of increase HCO3, 0.07 mmhg of pco2 will increase. In Resp .Acidosis (PH - DECREASED and PCO2 AND HCO3 INCREASED) Acute R.acidosis:- For every 10 mmhg increase in pco2 , 1 mmol/l Hco3 shld increase Chronic R acidosis:- for every 10 mmhg increase in pco2, Hco3 increases by 3.5mmol/l In Respiratory Alkalosis pH INCREASED, pco2 and Hco3 DECREASED Acute R.alkalosis :- for every 10 mmhg decrease in PCO2 , hco2 decreases by 2meq/l Chronic :- for very 10 mmhg decrease in PCO2 ,hco3 decreases by 10mmol/l Winters equation :- this equation helps u to determine ,what the expected PCO2 lloks like when there is a metabolic acidosis:- Anion GAP :- done always when the disorder is metabol Continue reading >>

## Acid Base Disorders

Arterial blood gas analysis is used to determine the adequacy of oxygenation and ventilation, assess respiratory function and determine the acid–base balance. These data provide information regarding potential primary and compensatory processes that affect the body’s acid–base buffering system. Interpret the ABGs in a stepwise manner: Determine the adequacy of oxygenation (PaO2) Normal range: 80–100 mmHg (10.6–13.3 kPa) Determine pH status Normal pH range: 7.35–7.45 (H+ 35–45 nmol/L) pH <7.35: Acidosis is an abnormal process that increases the serum hydrogen ion concentration, lowers the pH and results in acidaemia. pH >7.45: Alkalosis is an abnormal process that decreases the hydrogen ion concentration and results in alkalaemia. Determine the respiratory component (PaCO2) Primary respiratory acidosis (hypoventilation) if pH <7.35 and HCO3– normal. Normal range: PaCO2 35–45 mmHg (4.7–6.0 kPa) PaCO2 >45 mmHg (> 6.0 kPa): Respiratory compensation for metabolic alkalosis if pH >7.45 and HCO3– (increased). PaCO2 <35 mmHg (4.7 kPa): Primary respiratory alkalosis (hyperventilation) if pH >7.45 and HCO3– normal. Respiratory compensation for metabolic acidosis if pH <7.35 and HCO3– (decreased). Determine the metabolic component (HCO3–) Normal HCO3– range 22–26 mmol/L HCO3 <22 mmol/L: Primary metabolic acidosis if pH <7.35. Renal compensation for respiratory alkalosis if pH >7.45. HCO3 >26 mmol/L: Primary metabolic alkalosis if pH >7.45. Renal compensation for respiratory acidosis if pH <7.35. Additional definitions Osmolar Gap Use: Screening test for detecting abnormal low MW solutes (e.g. ethanol, methanol & ethylene glycol [Reference]) An elevated osmolar gap (>10) provides indirect evidence for the presence of an abnormal solute which is prese Continue reading >>

## Acid-base

Normal anion gap = 3-11 mEq/L. (8-16 if K is included in equation). Made upof unmeasured anions. Consist of proteins, mainly albumin. As a result areduction of albumin can reduce the baseline anion gap so that ahypoalbuminaemic patient may not have a high anion gap even in the presence of adisorder which usually produces an increased anion gap. Anion gap is reduced byapprox 2.5 mEq/L for every 10g/L fall in albumin. Alternatively a correctedvalue for a a normal anion gap (assuming K is included in calculation of aniongap) can be otained from: Corrected normal anion gap = 0.2[albumin] x 1.5[phosphate] where albumin is in g/L and phosphate in mmol/L - with hypokalaemia: classic distal (type 1) RTA - with hyperkalaemia: hyperkalaemic distal RTA , hypoaldosteronism (type 4) RTA Metabolic acidosis and respiratory alkalosis stimulation of respiratory centre by acidaemia causes a fall in PCO2 that in uncomplicated metabolic acidosis can be estimated from: lower than expected PCO2 indicates a superimposed respiratory alkalosis whereas a higher PCO2 indicates a respiratory acidosis. Equation only useful if plasma bicarbonate <20 mmol/L alternatively: a decrease in PCO2 of 0.16 kPa can be expected for a decrease in bicarbonate of 1 mmol/L. Ideally use nomogram complete respiratory compensation for primary metabolic acidosis does not occur respiratory compensation for acute acidosis tends to be somewhat greater than for chronic metabolic acidosis. Minimum level of PCO2 that can usually be attained is approx 1.3 kPa. Levels <2-2.7 kPa rarely maintained in chronic metabolic acidosis - combined hepatic and renal insufficiency (cirrhosis often associated with chronic respiratory alkalosis) - recent alcohol binge (alcoholic ketoacidosis + hyperventilation due to DTs) Metabolic acidosi Continue reading >>

## Have A Question - Step 2 Ck - Uworld Forums For Usmle, Abim, Abfm, And Nclex Forums

c.mixed respiratory and metabolic acidosis d.mixed metabolic acidosis and respiratory alkalosis my first impresion: acidic pH with low bicarbonate makes metabolic acidosis; normal Pco2 makes NO respiratory compensation....i choose answer a.; on explinations they said is c. why? because co2 should be 32 mmHG(after Winter formula); well...here is my question: if we are taking this explination as granted, then ALL the acid base disturbances should have compensation and my concern is how will look the noncompensated acid base disturbances???? that means we should not choose that answer where says 'compansation'; if anybody can give me a real and strong explanation, i will really apreciate it....thanks! Pco2 increase .7mmHg for every 1 mEq/L bicarbonate increase. In this case, Pco2 should be in range of 30 and 34mmHg. 40mmHg is normal Pco2 in individual but in acidosis, it should decrease if there is respiratory compensation. So the answer is mixed respiratory and metabolic acidosis. fantastic explanation and thank you for that....very similar to what offer uworld....still i got 1 more question: we ALWAYS have to see which is the respiratory compensation based on Winter formula....how it will look this scenario if we don't have respiratory compansation???? how i am supose to know WHEN we have and IF we have compensation???? you said in your comment that Pco2 should be 30 to 34 IF WE HAVE COMPENSATION!!!! my frustation is not with the explanation which i agree with it....my opinion: both answers are good...why? if you have compensation, Pco2 should be arround 32(jusy like you explain) but we don't have that; so we remain with 2 options: pure metabolic acidosis WITHOUT compensation or mixed metabolic and respiratory acidosis; if we don't have compensation, Pco2 should be norm Continue reading >>

## Acid-base Disorders - Renal - Medbullets Step 1

This patient'sarterial blood gas is consistent with metabolic acidosis with appropriate respiratory compensation, likely secondary to diabetic ketoacidosis. In patients with suspected acid-base disorders, it is important to analyze the arterial blood gas systematically. If the pH is low, the patient has acidemia. The presence of a low pH and low bicarbonate signifies that metabolic acidosis is the primary process. To determine whether or not the decrease in PCO2 represents an appropriate respiratory compensation, one should employ Winters formula: PCO2 = (1.5 x HCO3-) + 8 2. If PCO2 is within the range determined by the formula, it is considered to represent appropriate respiratory compensation. If the observed PCO2 is higher than that determined by the formula, there is mixed metabolic and respiratory acidosis; similarly, if the PCO2 is lower than that calculated by the formula, there is a mixed metabolic acidosis and respiratory alkalosis. Trachtenbarg reviews the clinical presentation of diabetic ketoacidosis (DKA). The following criteria are required for the diagnosis of DKA: plasma glucose concentration > 250 mg/dL, pH < 7.30, and bicarbonate 18 mEq/L or less. Beta-hydroxybutyrate is a more specific marker of ketoacidosis than serum ketones. Therapy begins with IV insulin and fluid resuscitation. Potassium levels must be carefully monitored, as these patients tend to have depleted potassium stores despite having normal values on laboratory testing, and will become hypokalemic as the acidosis is corrected. The underlying cause of DKA, such as infection or poor medical adherence, should be corrected. Schiraldi and Guiotto review the diagnosis of acid-base disorders. They advocate using the anion gap and "expected compensation" approach to determining the cause of an Continue reading >>

## Metabolic Acidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarbonate <22 mmol/L. Respiratory compensation occurs normally immediately, unless there is respiratory pathology. Pure metabolic acidosis is a term used to describe when there is not another primary acid-base derangement - ie there is not a mixed acid-base disorder. Compensation may be partial (very early in time course, limited by other acid-base derangements, or the acidosis exceeds the maximum compensation possible) or full. The Winter formula can be helpful here - the formula allows calculation of the expected compensating pCO2: If the measured pCO2 is >expected pCO2 then additional respiratory acidosis may also be present. It is important to remember that metabolic acidosis is not a diagnosis; rather, it is a metabolic derangement that indicates underlying disease(s) as a cause. Determination of the underlying cause is the key to correcting the acidosis and administering appropriate therapy[1]. Epidemiology It is relatively common, particularly among acutely unwell/critical care patients. There are no reliable figures for its overall incidence or prevalence in the population at large. Causes of metabolic acidosis There are many causes. They can be classified according to their pathophysiological origin, as below. The table is not exhaustive but lists those that are most common or clinically important to detect. Increased acid Continue reading >>

## Assessment Of Compensation: Boston And Copenhagen Methods - Deranged Physiology

Assessment of Compensation: Boston and Copenhagen Methods This page acts as a footnote to the "Boston vs. Copenhagen" chapter from Acid-Base Physiology by Kerry Brandis. The aforementioned chapter in my opinion remains the definitive resource on the topic. Brandis' chapter explores the epistemology of acid-base interpretation systems by means of which we might be able to determine whether a patient has a single or mixed acid base disorder; i.e. whether there is a purely metabolic or a purely respiratory disturbance, or some mixture of the two. As it happens, there are two well-accepted systems for doing this, each with its own merits and demerits. These are the Boston and Copenhagen methods of acid-base interpretation. There is also another not-so-well accepted system, the physicochemical method proposed by Peter Stewart - which possess a satisfying explanatory power as an instrument of academic physiology. Unfortunately, it is rather complicated, and difficult to apply at the bedside. Furthermore, there does not seem to be much of a difference in hard outcomes, regardless of which system one uses. Thus, this chapter will focus on the Boston and Copenhagen systems, which have equivalent validity as far as acid-base interpretation is concerned. "Which is the system I need to rote-learn to pass my primaries?" Such a question is expected from the fairweather intensivist, who will flee from the ICU as soon as a position opens in a more cushy training program. For the rest, one might remark that these analytical tools are all in common use, and any sufficiently advanced ICU trainee is expected to be intimately familiar with all of these systems. However, the time-poor exam candidate may need to focus their attention on the area which would yield the greatest number of marks Continue reading >>

## 9.3 Bedside Rules For Assessment Of Compensation

The method of assessing acid-base disorders discussed here uses a set of six rules which are used primarily to assess the magnitude of the patients compensatory response. These rules are now widely known and are soundly based experimentally. These rules are used at Step 4 of the method of Systematic Acid-Base Diagnosis outlined in Section 9.2.- (You should read section 9.1 & 9.2 before this section.) These rules are called 'bedside rules' because that can be used at the patient's bedside to assist in the assessment of the acid-base results. The rules should preferably be committed to memory - with practice this is not difficult. A full assessment of blood-gas results must be based on a clinical knowledge of the individual patient from whom they were obtained and an understanding of the pathophysiology of the clinical conditions underlying the acid-base disorder. Do not interpret the blood-gas results as an intellectual exercise in itself. It is one part of the overall process of assessing and managing the patient. A set of blood-gas and electrolyte results should NOT be interpreted without these initial clinical details. They cannot be understood fully without knowledge of the condition being diagnosed. Diagnosing a metabolic acidosis, for example, is by itself, often of little clinical use. What is really required is a more specific diagnosis of the cause of the metabolic acidosis (eg diabetic ketoacidosis, acute renal failure, lactic acidosis) and to initiate appropriate management. The acid-base analysis must be interpreted and managed in the context of the overall clinical picture. The snapshot problem: Are the results 'current'? Remember also that a set of blood gas results provides a snapshot at a particular point in time and the situation may have changed since Continue reading >>

## Metabolic Acidosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

(Video) Overview of Acid-Base Maps and Compensatory Mechanisms By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincent’s Ascension Health, Birmingham 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. Metabolic acidosis is acid accumulation due to Increased acid production or acid ingestion 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 ). Lactic acidosis (due to physiologic processes) Lactic acidosis (due to exogenous toxins) Toluene (initially high gap; subsequent excretion of metabolites normalizes gap) HIV nucleoside reverse transcriptase inhibitors Biguanides (rare except with acute kidney injury) Normal anion gap (hyperchloremic acidosis) Renal tubular acidosis, types 1, 2, and 4 The most common causes of a high anion gap metabolic acidosis are Ketoacidosis is a common complication of type 1 diabetes mellitus (see diabetic ketoacidosis ), but it also occurs with chronic alcoholism (see alcoholic ketoacidos Continue reading >>

## Bicarbonate Correction In Metabolic Acidosis Formula

Bicarbonate correction in metabolic acidosis formula 20. References 1. 5. The amount of bicarbonate req'd to correct a metabolic acidosis can be estimated from the following formula: A common transient cause is iatrogenic; correction of acute metabolic acidosis with sodium bicarbonate leaves a residual metabolic alkalosis. If metabolic acidosis is present, is there an increased anion gap? - can have an anion gap acidosis even with a normal anion gap if hypoalbuminemic (decrease in unmeasured anions). 4% (1 mmol/mL). 1mmol. If bicarbonate is used, A useful formula for cal-culating the bicarbonate requirement is: Winters' formula, named for Dr. , diarrhea) or from its titration to an anionic base that often can be converted back to bicarbonate, such as seen in diabetic ketoacidosis or lactic acidosis (Table 1). High Bicarbonate: The type of acidosis is categorized as either respiratory acidosis or metabolic acidosis, may be given oral sodium bicarbonate. 1. Too-rapid correction of formula for cal- improves the acidosis; A comprehensive review of metabolic acidosis. A graphic representation of the formula (Figure 5 in reference) shows that the apparent bicarbonate space increases quite markedly with acidemia but decreases veryModerate metabolic acidosis: 50 to 150 mEq sodium bicarbonate diluted in 1 L of D5W to be intravenously infused at a rate of 1 to 1. Metabolic acidosis can be formula: Corrected [Bicarbonate Metabolic Acidosis in Acute Myocardial Infarction amount of bicarbonate required for correction varied from 50 have a significant metabolic acidosis and have Help contents Stepwise correction of acidosis with frequent lab evaluation is preferred to avoid the poorly controlled metabolic acidosis. The study was aimed at detecting theIn patients with acute lactic ac Continue reading >>

## Additional Step In Abg Analysis

Michelle Kirschner , RN, MSN, APRN, CNP, CCRN The article Assessing Tissue Oxygenation (June 2002:2240) contains a comprehensive overview of arterial blood gas analysis, which will prove to be a valuable resource for nurses and other healthcare professionals in the intensive care environment. The steps outlined are useful in determining an acid-base imbalance involving either the metabolic or respiratory systems and the effectiveness of attempted compensation. However, severely ill patients who develop multiple organ failure frequently present with several acid-base abnormalities occurring simultaneously. Therefore, I routinely add an additional step in the analysis of arterial blood gases to determine if another primary acid-base process is present. The purpose of the additional step is to determine the expected compensation for the primary disorder. If the actual compensation falls within the calculated range, then a second disorder does not coexist. If the calculated value does not match the measured value, then a mixed disorder is present or compensation has not had time to occur. The expected compensation is calculated by using one of 4 formulas based on the primary process: metabolic acidosis, metabolic alkalosis, respiratory acidosis, or respiratory alkalosis. Metabolic conditions are generally compensated fairly quickly by the respiratory system by eliciting an alteration in the Pco2 level. The Winters formula predicts the expected degrees of compensation in a stable, steady-state metabolic disorder: If the actual Pco2 is higher than calculated with Winters formula, then a respiratory acidosis is mostly likely present in addition to the metabolic acid-base disorder. If the Pco2 is greater than 50 to 55 mm Hg, then respiratory acidosis is almost certainly presen Continue reading >>

## Paediatric Acid-base Disorders: A Case-based Review Of Procedures And Pitfalls

Paediatric acid-base disorders: A case-based review of procedures and pitfalls J Bryan Carmody , MD and Victoria F Norwood , MD Department of Pediatrics, Division of Pediatric Nephrology, University of Virginia, Charlottesville, Virginia, USA Correspondence: Dr J Bryan Carmody, Department of Pediatrics, Division of Pediatric Neprhology, University of Virginia, PO Box 800386, Charlottesville, Virginia 22903, USA. Telephone 434-924-2096, e-mail [email protected] , [email protected] Copyright 2013 Pulsus Group Inc. All rights reserved Acid-base disorders occur frequently in paediatric patients. Despite the perception that their analysis is complex and difficult, a straightforward set of rules is sufficient to interpret even the most complex disorders provided certain pitfalls are avoided. Using a case-based approach, the present article reviews the fundamental concepts of acid-base analysis and highlights common mistakes and oversights. Specific topics include the proper identification of the primary disorder; distinguishing compensatory changes from additional primary disorders; use of the albumin-corrected anion gap to generate a differential diagnosis for patients with metabolic acidosis; screening for mixed disorders with the delta-delta formula; recognizing the limits of compensation; use of the anion gap to identify hidden acidosis; and the importance of using information from the history and physical examination to identify the specific cause of a patients acid-base disturbance. Keywords: Acid-base equilibrium, Acid-base imbalances, Acidosis, Alkolosis, Blood Les troubles de lquilibre acido-basique sont frquents chez les patients dge pdiatrique. Mme si on les croit difficiles et complexes analyser, des rgles simples suffsent pour interprter mme les Continue reading >>