What Is The Compensation For Metabolic Acidosis?

Uncompensated, Partially Compensated, Or Combined Abg Problems

Arterial Blood Gas (ABG) analysis requires in-depth expertise. If the results are not understood right, or are wrongly interpreted, it can result in wrong diagnosis and end up in an inappropriate management of the patient. ABG analysis is carried out when the patient is dealing with the following conditions: • Breathing problems • Lung diseases (asthma, cystic fibrosis, COPD) • Heart failure • Kidney failure ABG reports help in answering the following questions: 1. Is there acidosis or alkalosis? 2. If acidosis is present, whether it is in an uncompensated state, partially compensated state, or in fully compensated state? 3. Whether acidosis is respiratory or metabolic? ABG reports provide the following descriptions: PaCO2 (partial pressure of dissolved CO2 in the blood) and PaO2 (partial pressure of dissolved O2 in the blood) describe the efficiency of exchange of gas in the alveolar level into the blood. Any change in these levels causes changes in the pH. HCO3 (bicarbonate in the blood) maintains the pH of the blood within normal range by compensatory mechanisms, which is either by retaining or increasing HCO3 excretion by the kidney. When PaCO2 increases, HCO3 decreases to compensate the pH. The following table summarizes the changes: ABG can be interpreted using the following analysis points: Finding acidosis or alkalosis: • If pH is more it is acidosis, if pH is less it is alkalosis. Finding compensated, partially compensated, or uncompensated ABG problems: • When PaCO2 is high, but pH is normal instead of being acidic, and if HCO3 levels are also increased, then it means that the compensatory mechanism has retained more HCO3 to maintain the pH. • When PaCO2 and HCO3 values are high but pH is acidic, then it indicates partial compensation. It means t Continue reading >>

Acute Acid-base Disorders. 2. Specific Disturbances.

Acute acid-base disorders. 2. Specific disturbances. Evaluation of the acid-base status of the body requires measurement of bicarbonate (total carbon dioxide) concentration, pH, and partial pressure of CO2 in arterial blood. Calculation of standard bicarbonate and base excess or deficit is not necessary. The normal concentration of free hydrogen ions (H+) is approximately 40 millimoles/liter, which is equivalent to a pH of 7.4. The normal load of fixed acids is 50 to 80 millimoles in 24 hours. A steady state is maintained by excretion of an equal amount of H+ by the kidneys, which at the same time regenerate bicarbonate to replenish buffer stores. Renal excretion of H+ is in the form of titratable acid and ammonium. Synthesis of ammonia can increase severalfold under the stimulus of acidosis. This is the chief mechanism of long-term compensation. Metabolic acidosis can be due to an excessive acid load (endogenous or exogenous), impaired renal excretion of H+, or bicarbonate loss. Determination of the "anion gap" (unmeasured anions) helps to establish the mechanism of acidosis. Acidosis with a normal anion gap is due to either bicarbonate loss or ingestion of certain chloride salts. A gap larger than normal indicates the presence in the body of acids other than acidfying chloride salts. Management of metabolic acidosis requires accurate diagnosis, clear understanding of the mechansim, and individualized treatment. Metabloic alkalosis is due to loss of H+ (usually from stomach or kidneys) or ingestion of alkali. Measurement of urinary chloride helps establish the mechanism of alkalosis. In saline-responsive alkalosis, the urinary chloride level is very low. This is usually due to gastric loss of H+, and the condition responds to administration of saline solution. When th 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 >>

Intro To Arterial Blood Gases, Part 2

Arterial Blood Gas Analysis, Part 2 Introduction Acute vs. Chronic Respiratory Disturbances Primary Metabolic Disturbances Anion Gap Mixed Disorders Compensatory Mechanisms Steps in ABG Analysis, Part II Summary Compensatory Mechanisms Compensation refers to the body's natural mechanisms of counteracting a primary acid-base disorder in an attempt to maintain homeostasis. As you learned in Acute vs. Chronic Respiratory Disturbances, the kidneys can compensate for chronic respiratory disorders by either holding on to or dumping bicarbonate. With Chronic respiratory acidosis: Chronic respiratory alkalosis: the kidneys hold on to bicarbonate the kidneys dump bicarbonate With primary metabolic disturbances, the respiratory system compensates for the acid-base disorder. The lungs can either blow off excess acid (via CO2) to compensate for metabolic acidosis, or to a lesser extent, hold on to acid (via CO2) to compensate for metabolic alkalosis. With Metabolic acidosis: Metabolic alkalosis: ventilation increases to blow off CO2 ventilation decreases to hold on to CO2 The body's response to metabolic acidosis is predictable. With metabolic acidosis, respiration will increase to blow off CO2, thereby decreasing the amount of acid in the blood. Recall that with metabolic acidosis, central chemoreceptors are triggered by the low pH and increase the drive to breathe. For now, it is only important to learn (qualitatively) that there is a predictable compensatory response to metabolic acidosis. Later, during your 3rd or 4th year rotations, you might learn how to (quantitatively) determine if the compensatory response to metabolic acidosis is appropriate by using the Winter's Formula. The body's response to metabolic alkalosis is not as complete. This is because we would need to hypov Continue reading >>

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 >>

5.5 Metabolic Acidosis - Compensation

Acid-Base Physiology 5.5.1 Hyperventilation Compensation for a metabolic acidosis is hyperventilation to decrease the arterial pCO2. This hyperventilation was first described by Kussmaul in patients with diabetic ketoacidosis in 1874. The metabolic acidosis is detected by both the peripheral and central chemoreceptors and the respiratory center is stimulated. The initial stimulation of the central chemoreceptors is due to small increases in brain ISF [H+]. The subsequent increase in ventilation causes a fall in arterial pCO2 which inhibits the ventilatory response. Maximal compensation takes 12 to 24 hours The chemoreceptor inhibition acts to limit and delay the full ventilatory response until bicarbonate shifts have stabilised across the blood brain barrier. The increase in ventilation usually starts within minutes and is usually well advanced at 2 hours of onset but maximal compensation may take 12 to 24 hours to develop. This is �maximal� compensation rather than �full� compensation as it does not return the extracellular pH to normal. In situations where a metabolic acidosis develops rapidly and is short-lived there is usually little time for much compensatory ventilatory response to occur. An example is the acute and sometimes severe lactic acidosis due to a prolonged generalised convulsion: this corrects due to rapid hepatic uptake and metabolism of the lactate following cessation of convulsive muscular activity, and hyperventilation due to the acidosis does not occur. The expected pCO2 at maximal compensation can be calculated from a simple formula The arterial pCO2 at maximal compensation has been measured in many patients with a metabolic acidosis. A consistent relationship between bicarbonate level and pCO2 has been found. It can be estimated from the Continue reading >>

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 >>

Metabolic Acidosis

Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms[edit] Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia Continue reading >>

Metabolic Acidosis Treatment & Management

Approach Considerations Treatment of acute metabolic acidosis by alkali therapy is usually indicated to raise and maintain the plasma pH to greater than 7.20. In the following two circumstances this is particularly important. When the serum pH is below 7.20, a continued fall in the serum HCO3- level may result in a significant drop in pH. This is especially true when the PCO2 is close to the lower limit of compensation, which in an otherwise healthy young individual is approximately 15 mm Hg. With increasing age and other complicating illnesses, the limit of compensation is likely to be less. A further small drop in HCO3- at this point thus is not matched by a corresponding fall in PaCO2, and rapid decompensation can occur. For example, in a patient with metabolic acidosis with a serum HCO3- level of 9 mEq/L and a maximally compensated PCO2 of 20 mm Hg, a drop in the serum HCO3- level to 7 mEq/L results in a change in pH from 7.28 to 7.16. A second situation in which HCO3- correction should be considered is in well-compensated metabolic acidosis with impending respiratory failure. As metabolic acidosis continues in some patients, the increased ventilatory drive to lower the PaCO2 may not be sustainable because of respiratory muscle fatigue. In this situation, a PaCO2 that starts to rise may change the plasma pH dramatically even without a significant further fall in HCO3-. For example, in a patient with metabolic acidosis with a serum HCO3- level of 15 and a compensated PaCO2 of 27 mm Hg, a rise in PaCO2 to 37 mm Hg results in a change in pH from 7.33 to 7.20. A further rise of the PaCO2 to 43 mm Hg drops the pH to 7.14. All of this would have occurred while the serum HCO3- level remained at 15 mEq/L. In lactic acidosis and diabetic ketoacidosis, the organic anion can r Continue reading >>

Metabolic Acidosis | Pathway Medicine

Metabolic Acidosis is a pathophysiological category of acidosis that refers to any cause of decreased ECF pH not due to a ventilatory defect (i.e. Respiratory Acidosis). Although the primary metabolic disturbance can cause a significant decrease in blood pH, respiratory compensatory mechanisms can largely correct the pH over several hours. The fundamental primary disturbance in a metabolic acidosis is a decrease in the levels of ECF bicarbonate concentration ([HCO3-]). Decreased bicarbonate results in an misalignment of the Henderson-Hasselbalch Equation for the bicarbonate buffer which largely determines the pH of the extracellular fluid. Mathematically, the reduced ECF pH results from an increase in the ratio between the partial pressure of arterial carbon dioxide (PaCO2) relative to the ECF concentration of bicarbonate ([HCO3-]). More colloquially, metabolic acidoses are caused by a pathologic consumption of the weak base form of the bicarbonate buffer, that is bicarbonate (HCO3-), resulting in a decrease in ECF pH. Metabolic Acidoses can be compensated by the actions of the lungs which serve to realign the bicarbonate buffer Henderson-Hasselbalch Equation over a period of hours. As described in Respiratory Acid-Base Control , the lungs respond to acidosis by increasing alveolar ventilation , essentially a physiological hyperventilation, which in turn reduces the PaCO2. The decreased PaCO2 realigns the Henderson-Hasselbalch Equation for the bicarbonate buffer and thus largely corrects the ECF pH. Consequently, a respiratory-compensated metabolic acidosis is characterized by decreased levels of ECF bicarbonate (caused by the primary metabolic disturbance) as well as decreased levels of PaCO2 (caused by the respiratory compensation). More colloquially, the lungs compe Continue reading >>

Acid-base Disorders - 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 Vincents Ascension Health, Birmingham Acid-base disorders are pathologic changes in carbon dioxide partial pressure (Pco2) or serum bicarbonate (HCO3) that typically produce abnormal arterial pH values. Acidosis refers to physiologic processes that cause acid accumulation or alkali loss. Alkalosis refers to physiologic processes that cause alkali accumulation or acid loss. Actual changes in pH depend on the degree of physiologic compensation and whether multiple processes are present. Primary acid-base disturbances are defined as metabolic or respiratory based on clinical context and whether the primary change in pH is due to an alteration in serum HCO3 or in Pco2. Metabolic acidosis is serum HCO3< 24 mEq/L. Causes are Metabolic alkalosis is serum HCO3> 24 mEq/L. Causes are Respiratory acidosis is Pco2> 40 mm Hg (hypercapnia). Cause is Decrease in minute ventilation (hypoventilation) Respiratory alkalosis is Pco2< 40 mm Hg (hypocapnia). Cause is Increase in minute ventilation (hyperventilation) Compensatory mechanisms begin to correct the pH (see Table: Primary Changes and Compensations in Simple Acid-Base Disorders ) whenever an acid-base disorder is present. Compensation cannot return pH completely to normal and never overshoots. A simple acid-base disorder is a single acid-base disturbance with its accompanying compensatory response. Mixed acid-base disorders comprise 2 primary disturbances. Compensatory mechanisms for acid-base disturbances cannot return pH completely to normal and never overshoot. Primary Changes and Compensations in Simple Acid-Base Disorders 1.2 mm Hg decrease in Pco2 for every 1 mmol/L decrease in HC Continue reading >>

Time Course For Development Of Respiratory Compensation In Metabolic Acidosis

Respiration in Galleria mellonella follows a sigmoid curve with changing temperature in much the same manner as that of corresponding stages of Phormia regina. At 30C the respiration of 2- and 5-day-old Galleria pupae and female adults becomes limited by some oxygen concentration between 10% and 5%. Seven-day-old pupae apparently are more dependent on the oxygen tension, and larvae are more ... [Show full abstract] dependent on the ambient oxygen concentration than any other stage. Similar response to lowered oxygen concentration by comparable stages of Galleria and Phormia indicates that adjustment of spiracular area alone does not determine the degree of dependence of the insect on ambient oxygen concentration.1.Die Atmung eines jeden Stadiums von Galleria mellonella folgt bei Temperaturnderung einer sigmoidalen Kurve fast in der gleichen Weise wie die entsprechender Stadien von Phormia regina (Keister & Buck 1961).2.Die Atmung von 2 und 5 Tage alten Galleria-Puppen und weiblichen Imagines wird (bei 30) von Sauerstoffkonzentrationen von etwa 10 bis 5% begrenzt. 7 Tage alte Puppen sind offensichtlich strker von einer hheren Sauerstoffspannung abhngig. Galleria-Larven sind von der Sauerstoffkonzentration der Umgebung viel strker abhngig als jedes andere Stadium. Ein unerklrtes Ergebnis ist die den Verbrauch herabsetzende Wirkung eines Luftberflusses berflusses auf die Atmung der erwachsenen Mnnchen.3.Offensichtliche Geschlechtsunterschiede im Sauerstoffverbrauch wurden in den Versuchen durchgehend festgestellt, wobei die Mnnchen gewhnlich die hheren Respirationsraten aufwiesen. Die Differenzen sind jedoch nur bei Temperaturen zwischen 30 und 45 statistisch signifikant.4.Die hnliche Reaktion vergleichbarer Stadien von Galleria und Phormia auf herabgesetzte Sauerstoffkon Continue reading >>

Perfecting Your Acid-base Balancing Act

When it comes to acids and bases, the difference between life and death is balance. The body’s acid-base balance depends on some delicately balanced chemical reactions. The hydrogen ion (H+) affects pH, and pH regulation influences the speed of cellular reactions, cell function, cell permeability, and the very integrity of cell structure. When an imbalance develops, you can detect it quickly by knowing how to assess your patient and interpret arterial blood gas (ABG) values. And you can restore the balance by targeting your interventions to the specific acid-base disorder you find. Basics of acid-base balance Before assessing a patient’s acid-base balance, you need to understand how the H+ affects acids, bases, and pH. An acid is a substance that can donate H+ to a base. Examples include hydrochloric acid, nitric acid, ammonium ion, lactic acid, acetic acid, and carbonic acid (H2CO3). A base is a substance that can accept or bind H+. Examples include ammonia, lactate, acetate, and bicarbonate (HCO3-). pH reflects the overall H+ concentration in body fluids. The higher the number of H+ in the blood, the lower the pH; and the lower the number of H+, the higher the pH. A solution containing more base than acid has fewer H+ and a higher pH. A solution containing more acid than base has more H+ and a lower pH. The pH of water (H2O), 7.4, is considered neutral. The pH of blood is slightly alkaline and has a normal range of 7.35 to 7.45. For normal enzyme and cell function and normal metabolism, the blood’s pH must remain in this narrow range. If the blood is acidic, the force of cardiac contractions diminishes. If the blood is alkaline, neuromuscular function becomes impaired. A blood pH below 6.8 or above 7.8 is usually fatal. pH also reflects the balance between the p Continue reading >>

Compensation In Acid/base Imbalances

Respiratory compensation for metabolic acidosis (HNC excess) produces systemic hypocapnia (low PCO2). CO2 diffuses from CSF to the body causing the CSF pH to increase. This reduces the central chemoreceptor-stimulated ventilation, partly off-setting the increased stimulation of the peripheral chemoreceptors caused by the low arterial pH. Ventilatory stimulation (low arterial pH acting on peripheral chemoreceptors) Ventilatory inhibition (high CSF pH acting on the central chemoreceptor). What is the overall effect of the ventilatory stimulation and ventilatory inhibition? Respiratory compensation stops short of completely correcting the pH. Respiratory compensation cannot fully restore pH, but the kidney can (for metabolic acidosis anyway). For each H+ that is excreted in the urine (after all of the filtered HCO3- has been reabsorbed), and during ammonia production, new HCO3- enters the body. This added HCO3- titrates excess H+ and over 3 to 4 days the added HCO3- restores pH to 7.4. Renal Compensation Seen on Davenport nomogram Trajectory is along the RC line because as HCO3- is slowly added the pH changes, reducing the stimulation of the respiratory system. Summary of Renal Compensation and Respiratory Compensation PCO2 changes back to normal (renal and respiratory compensation working at the same time) pH and HCO3- change back to normal by sliding up or down the RC line in the Davenport nomogram We can estimate the amount of NC acid that caused a metabolic acidosis by seeing how much HCO3-, HB-, and other NC bases would be needed to fix the problem completely. Also, We can estimate the amount of base needed to restore pH back to normal by hypothetically continuing respiratory compensation. How is base excess/deficit measured on the Davenport nomogram? Base deficit 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 >>