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Metabolic Acidosis Compensation Calculator

Acid Base Disorders

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 >>

Deciphering Acid-base Disorders

Deciphering Acid-base Disorders

Derangements in acid-base status are commonly discovered on routine emergency department evaluation and often suggest the presence of severe underlying disease. Many acute conditions can disrupt homeostatic mechanisms used to buffer and excrete acid, and these changes may necessitate immediate intervention. When you discover a patient with an abnormal pH, what is your approach to the diagnosis? Large amounts of fixed and volatile acid are produced as normal byproducts of cellular metabolism. In addition to excretion of these byproducts via the lungs and kidneys, physiologic pH is maintained using carbon dioxide and bicarbonate as buffers. The balance of serum PCO2 and HCO3 directly impact pH, and disruption of this ratio results in primary acidemia or alkalemia, depending on the direction of the change. Notably, acidemia and alkalemia describe changes in serum pH, whereas acidosis and alkalosis refer to the clinical conditions underlying those changes. These conditions can be either metabolic or respiratory in etiology, leading to 4 categories of primary acid-base disorders. In response to this primary change, compensatory mechanisms attempt to drive the pH toward normal by keeping the PCO2/HCO3 ratio constant. The degree of compensation is related to the chronicity of the primary disorder, but does not generally restore the pH to normal. To add to the complexity, patients can have more than one primary disorder. Features of each disorder are detailed as follows, which assumes ABGs are used: * Respiratory compensation becomes less effective for chronic metabolic disorders ** There is conflicting data regarding reliable elevation in AG from isolated lactic acidosis *** For isolated respiratory processes only Checklist: Evaluating Acid Base Disturbances Acid-base physiol Continue reading >>

Interpretation Of Arterial Blood Gas

Interpretation Of Arterial Blood Gas

Go to: Introduction Arterial blood gas (ABG) analysis is an essential part of diagnosing and managing a patient’s oxygenation status and acid–base balance. The usefulness of this diagnostic tool is dependent on being able to correctly interpret the results. Disorders of acid–base balance can create complications in many disease states, and occasionally the abnormality may be so severe so as to become a life-threatening risk factor. A thorough understanding of acid–base balance is mandatory for any physician, and intensivist, and the anesthesiologist is no exception. The three widely used approaches to acid–base physiology are the HCO3- (in the context of pCO2), standard base excess (SBE), and strong ion difference (SID). It has been more than 20 years since the Stewart’s concept of SID was introduced, which is defined as the absolute difference between completely dissociated anions and cations. According to the principle of electrical neutrality, this difference is balanced by the weak acids and CO2. The SID is defined in terms of weak acids and CO2 subsequently has been re-designated as effective SID (SIDe) which is identical to “buffer base.” Similarly, Stewart’s original term for total weak acid concentration (ATOT) is now defined as the dissociated (A-) plus undissociated (AH) weak acid forms. This is familiarly known as anion gap (AG), when normal concentration is actually caused by A-. Thus all the three methods yield virtually identical results when they are used to quantify acid–base status of a given blood sample.[1] Continue reading >>

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

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 >>

Arterial Blood Gas Analysis: Example Set 2

Arterial Blood Gas Analysis: Example Set 2

Arterial Blood Gas Analysis: Example Set 2 You are working in the emergency room when the paramedics bring in a 45 year-old man who was found down in Pioneer Square. He is somnolent but arouseable. He has emesis on his shirt. He is hypotensive and tachycardic. Labs are drawn and reveal the following: Step 2: The PCO2 is low (respiratory alkalosis) and the bicarbonate is low (metabolic acidosis). Therefore, the metabolic acidosis is the primary process. Step 3: The serum anion gap is elevated at 29. There is, therefore, an elevated anion gap acidosis. Step 4: The respiratory alkalosis is the compensatory process for the metabolic acidosis. The Delta Gap = Measured SAG Normal SAG = 29 12 = 17 Calculate the Delta Delta: Delta Gap + measured bicarbonate = 17 + 12 = 29 Since the Delta Delta is above a normal bicarbonate level, there is a concurrent metabolic alkalosis at work. The patient has a primary elevated anion gap acidosis with respiratory compensation (which is not complete) and a concurrent metabolic alkalosis. You would need to sort through the differential diagnosis for an elevated anion gap acidosis to identify the cause of that problem. The metabolic alkalosis is likely due to vomiting. A 60 year-old man was recently in the hospital for treatment of aspiration pneumonia for which he as treated with levofloxacin and clindamycin. One week later, he presents to the ER with severe diarrhea, abdominal pain and hypotension. Step 2: The PCO2 is low (respiratory alkalosis) and the bicarbonate is low (metabolic acidosis). Therefore, the metabolic acidosis is the primary process. Step 3: The serum anion gap is elevated at 20. There is, therefore, an elevated anion gap acidosis. Step 4: The respiratory alkalosis is the compensatory process for the metabolic acidosis. The Continue reading >>

Winters Formula Calculator For Metabolic Acidosis

Winters Formula Calculator For Metabolic Acidosis

Winters Formula Calculator For Metabolic Acidosis Establishes the level of PCO2 compensation in metabolic and mixed acidosis cases, based on bicarbonate. Read more about the Winters formula and when to use it, in the text below the form. Winters formula calculator uses the bicarbonate level (HCO3-) to determine the partial CO2 pressure (PCO2) compensation in patients with metabolic and mixed acidosis. The formula was developed by Dr Winters specifically to predict the level of respiratory compensation that would be necessary to recover from acidosis. The formula used by this metabolic acidosis compensation calculator is: Which leads to the creation of a compensation interval between 1.5 x HCO3- + 6 and 1.5 x HCO3- + 10. To embed this calculator, please copy this code and insert it into your desired page: To Save This Calculator As A Favourite You Must Be Logged In... Creating an account is free and takes less than 1 minute. Steps on how to print your input & results: 1. Fill in the calculator/tool with your values and/or your answer choices and press Calculate. 2. Then you can click on the Print button to open a PDF in a separate window with the inputs and results. You can further save the PDF or print it. Please note that once you have closed the PDF you need to click on the Calculate button before you try opening it again, otherwise the input and/or results may not appear in the pdf. In cases of metabolic acidosis, medical professionals may be required to evaluate PCO2 compensation in connection with the level of bicarbonate [HCO3-]. The Winters formula calculator provides the lower and upper values of partial CO2 pressure in mmHg: Which means that the creation of a compensation interval between 1.5 x HCO3- + 6 and 1.5 x HCO3- + 10. The rule is that for every 1 mEq/L Continue reading >>

Acid Base Calculation Made Easy !

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 >>

Abg Interpretation

Abg Interpretation

Arterial blood gas (ABG) interpretation is something many medical students find difficult to grasp (we’ve been there). We’ve created this guide, which aims to provide a structured approach to ABG interpretation whilst also increasing your understanding of each results relevance. The real value of an ABG comes from its ability to provide a near immediate reflection of the physiology of your patient, allowing you to recognise and treat pathology more rapidly. To see how to perform an arterial blood gas check out our guide here. If you want to put your ABG interpretation skills to the test, check out our ABG quiz here. Normal ranges pH: 7.35 – 7.45 PaCO2: 4.7-6.0 kPa PaO2: 11-13 kPa HCO3-: 22-26 mEg/L Base excess: -2 to +2 mmol/L Patient’s clinical condition Before getting stuck into the details of the analysis, it’s important to look at the patient’s current clinical status, as this provides essential context to the ABG result. Below are a few examples to demonstrate how important context is when interpreting an ABG. A normal PaO2 in a patient on high flow oxygen – this is abnormal as you would expect the patient to have a PaO2 well above the normal range with this level of oxygen therapy A normal PaCO2 in a hypoxic asthmatic patient – a sign they are tiring and need ITU intervention A very low PaO2 in a patient who looks completely well, is not short of breath and has normal O2 saturations – likely a venous sample Oxygenation (PaO2) Your first question when looking at the ABG should be “Is this patient hypoxic?” (because this will kill them long before anything else does). PaO2 should be >10 kPa on air in a healthy patient If the patient is receiving oxygen therapy their PaO2 should be approximately 10kPa less than the % inspired concentration / FiO Continue reading >>

Acid Base Disorders

Acid Base Disorders

Acid base disorders 1. What is normal pH? Normal Values pH = 7.38 - 7.42 [H+] = 40 nM/L for a pH of 7.4 PaCO2 = 40 mm Hg [HCO3] = 24 meq/L 2. What is the definition for acid base disorder? Acid base disorder is considered present when there is abnormality in HCO3 or PaCO2 or pH. 3. What does acidosis or alkalosis refer to? Acidosis and alkalosis refer to in-vivo derangement's and not to any change in pH. 4. What does acidemia or alkalemia refer to? Acidemia (pH < 7.38) and Alkalemia (pH >7.42) refer to derangement's of blood pH. 5. Which organs are key players in maintaining acid base balance? Kidney, Respiratory system and Central nervous system play a key roles in maintaining the acid base status. 6. What are the primary acid base disorders? Primary acid base disorders Metabolic acidosis Metabolic alkalosis Respiratory acidosis Respiratory alkalosis 7. When would you consider metabolic acidosis? Metabolic acidosis: loss of [HCO3] 0r addition of [H+] 8. When would you consider metabolic alkalosis? Metabolic alkalosis: loss of [H+] or addition of [HCO3] 9. When would you consider respiratory acidosis? Respiratory acidosis: increase in pCO2 10. When would you consider respiratory alkalosis? Respiratory alkalosis : decrease in pCO2 11. What are the required lab values and historical information you need to assess acid base disorders? Recquired lab values/information Arterial blood gases: pH, PaCO2,calculated bicarb Electrolytes: Na, K, Cl, HCO3 BUN, Glucose, Creatinine Clinical history 12. What are anions? List the anions? Anions Chloride Bicarbonate(Total CO2) Proteins Organic acids Phosphates Sulfates 13. What are cations? List the cations? Cations Sodium Potassium Calcium Magnesium 14. What is anion gap? Anion gap (AG) Electrochemical balance: the total anions are the Continue reading >>

Metabolic Acidosis Treatment & Management

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 >>

Arterial Blood Gas (abg) Analyzer

Arterial Blood Gas (abg) Analyzer

This analyzer should not substitute for clinical context. Sodium and chloride are required for anion gap calculation. While the analyzer can often help with analysis, the history of the patient is critical for accurate interpretation. NOTE: Normal albumin levels are typically 4 g/dL in US units and 40 g/L in SI units. A venous blood gas often correlates well with arterial blood gas findings (except for PaO2) unless values are extremely abnormal, and can often be used successfully as a screening tool. This tool, developed by Jonathan Chen, MD first determines the primary process by looking at the pH and the PCO2. It then calculates compensations to determine chronicity, compensatory, and co-existing acid-base disturbances. Diabetic Ketoacidosis (check serum ketones) Propylene Glycol (in BZD drips) or Paraldehydes Oxoporin (reflects fatty liver damage from glutathione consumption, e.g. acetaminophen toxicity) Renal Tubular Acidosis (Type 1 Distal or Type 2 Proximal) Jonathan Chen, MD, PhD is a research fellow in medical informatics, based at the Veteran Affairs Hospital in Palo Alto and Stanford University. He completed the Stanford Internal Medicine residency program and was in the Medical Scientist Training Program (MSTP) and Biomedical Informatics Training (BIT) program at UC Irvine. Dr. Chen co-founded Reaction Explorer, LLC, which offers a unique system for teaching complex problem-solving in organic chemistry with the aid of expert system technology. To view Dr. Jonathan Chen's publications, visit PubMed 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 >>

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 >>

Winters Formula For Metabolic Acidosis Compensation Calculator

Winters Formula For Metabolic Acidosis Compensation Calculator

Winters Formula for Metabolic Acidosis Compensation Calculator This Winters formula for metabolic acidosis compensation calculator checks metabolic and mixed acidosis cases and establishes the level of PCO2 compensation. Discover more about the formula used and the situations that require it below the form. How does this Winters formula for metabolic acidosis compensation calculator work? This is a tool designed to help clinicians and any medical personnel evaluate PCO2 compensation in connection with the level of bicarbonate [HCO3-]. The form is very simple to use and only requires inputting bicarbonate in mEq/L and press calculate. The result will be displayed as an interval with the lower and upper values of partial CO2 pressure in mmHg. The formula used by this metabolic acidosis compensation calculator is explained below: Which means the interval between: 1.5 x HCO3- + 6 and 1.5 x HCO3- + 10 As a rule of thumb, there is a 1.2 mmHg PCO2 reduction for every 1 mEq/L reduction of plasma bicarbonate but only to a minimum of 10 - 15 mmHg. Taking an example, it shows that in order to compensate for a plasma concentration of HCO3- of 9 mEq/L it would be required a partial pressure of CO2 between 19.5 and 23.5 mmHg. The patients data is then compared to the computed value: If the value retrieved in patients data corresponds, this means that the respiratory compensation is adequate. If the value is higher this is indicative of primary respiratory acidosis and if the value is lower than the calculated value, it is indicative of primary respiratory alkalosis. However, the Winters formula is used mostly for metabolic acidosis and in the second case a different set of equations should be used as provided below: PCO2 = 0.7 x HCO3- + 20 +/- 5 mmHg meaning the interval between 0.7 Continue reading >>

5.5 Metabolic Acidosis - Compensation

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 >>

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