diabetestalk.net

Normal Anion Gap Metabolic Acidosis Wiki

File:cat Mudpiles - Causes Of High Anion-gap Metabolic Acidosis.svg

File:cat Mudpiles - Causes Of High Anion-gap Metabolic Acidosis.svg

File:Cat mudpiles - causes of high anion-gap metabolic acidosis.svg DescriptionCat mudpiles - causes of high anion-gap metabolic acidosis.svg English: Causes of high anion-gap metabolic acidosis Diabetic ketoacidosis, Alcoholic ketoacidosis, Starvation ketoacidosis Paracetamol/Acetaminophen, Phenformin, Paraldehyde Iron, Isoniazid, Inborn errors of metabolism Ethanol (due to lactic acidosis), Ethylene glycol This SVGdiagram uses embedded textthat can be easily translated using a text editor. Learn more . I, the copyright holder of this work, hereby publish it under the following license: This file is made available under the Creative Commons CC0 1.0 Universal Public Domain Dedication . The person who associated a work with this deed has dedicated the work to the public domain by waiving all of his or her rights to the work worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law. You can copy, modify, distribute and perform the work, even for commercial purposes, all without asking permission. Commons Zero, Public Domain Dedicationfalsefalse Click on a date/time to view the file as it appeared at that time. This file contains additional information such as Exif metadata which may have been added by the digital camera, scanner, or software program used to create or digitize it. If the file has been modified from its original state, some details such as the timestamp may not fully reflect those of the original file. The timestamp is only as accurate as the clock in the camera, and it may be completely wrong. Continue reading >>

Surgical Procedures/acid Base Disorder

Surgical Procedures/acid Base Disorder

(Usually in clinical practice, H+ concentration is expressed as pH.) PaCO2 (Arterial CO2 concentration normal = 3545 mm Hg). HCO3 (Serum electrolytes normal = 2231 mmol/liter). Acidosis is a process that causes the accumulation of acid. Alkalosis is a process that causes the accumulation of alkali. The most common causes in the surgical practice include: Diuretic therapy (e.g., contraction alkalosis). Acid loss through GI secretions (e.g., nasogastric suctioning, vomiting). Exogenous administration of HCO3 or HCO3 precursors (e.g., citrate in blood). Chloride-unresponsive metabolic alkalosis is comparatively less common and includes: Renal tubular Cl wasting (Bartters syndrome) Measurement of urinary chloride concentration. Suggestive causes of the metabolic alkalosis if Urine Cl concentration is <15 mmol/liter: Sughgestive causes of the metabolic alkalosis if Urine Cl concentration is > 20 mmol/liter: Treatment principles in metabolic alkalosis:[ edit ] Removing and identifying underlying causes, Discontinuing exogenous alkali, repairing Cl, K+, and volume deficits. Correction of volume deficits (can be used 0.9% NaCl) and hypokalemia. H2-receptor antagonists or other acid-suppressing medications can be used after vomiting or nasogastric suctioning. Acetazolamide (5 mg/kg/day IV or PO) can be used. Eases fluid mobilization while decreasing renal HCO3 reabsorption. Tolerance to this diuretic may develop after 23 days. Ammonium chloride (NH4Cl) can be used in severe alkalemia (HCO3 >40 mmol/liter; rate not exceeding 5 ml/minute). Approximately one-half of the calculated volume of NH4Cl is usually administered and the acid-base status and Cl concentration is usually rechecked to determine the need of further treatment. Hepatic failure is contraindication for NH4Cl. HCl m Continue reading >>

3.3 The Delta Ratio

3.3 The Delta Ratio

This Delta Ratio is sometimes useful in the assessment of metabolic acidosis 1,2,3,4 . As this concept is related to the anion gap (AG) and buffering, it will be discussed here before a discussion of metabolic acidosis. The Delta Ratio is defined as: Delta ratio = (Increase in Anion Gap / Decrease in bicarbonate) Others 5 have used the delta gap (defined as rise in AG minus the fall in bicarbonate), but this uses the same information as the delta ratio and has does not offer any advantage over it. In order to understand this, consider the following: If one molecule of metabolic acid (HA) is added to the ECF and dissociates, the one H+ released will react with one molecule of HCO3- to produce CO2 and H2O. This is the process of buffering. The net effect will be an increase in unmeasured anions by the one acid anion A- (ie anion gap increases by one) and a decrease in the bicarbonate by one. Now, if all the acid dissociated in the ECF and all the buffering was by bicarbonate, then the increase in the AG should be equal to the decrease in bicarbonate so the ratio between these two changes (which we call the delta ratio) should be equal to one. The delta ratio quantifies the relationship between the changes in these two quantities. If the AG was say 26 mmols/l (an increase of 14 from the average value of 12), it might be expected that the HCO3- would fall by the same amount from its usual value (ie 24 minus 14 = 10mmols/l). If the actual HCO3- value was different from this it would be indirect evidence of the presence of certain other acid-base disorders (see Guidelines below). A problem though: the above assumptions about all buffering occurring in the ECF and being totally by bicarbonate are not correct.Fifty to sixty percent of the buffering for a metabolic acidosis occ Continue reading >>

Wikitox - 2.2.5.2.5 Methanol

Wikitox - 2.2.5.2.5 Methanol

Methanol (methyl alcohol, wood spirits) is used as a fuel in high performance engines, solvents, as an antifreeze or window cleaner. Methanol is also used to fortify illicit spirits. Methanol is a colourless, flammable solution with a slightly alcoholic smell. Almost all significant exposures occur via ingestion, but methanol can also be absorbed via inhalation and through the skin. Small amounts of methanol are ingested with foods such as fresh fruit juices and vegetables. Methanol is a natural fermentation product found in all spirits. Serum methanol concentrations rise following binge drinking and are thought to be one cause of a hangover. Methanol toxicity produces a raised anion-gap metabolic acidosis, ocular and central nervous system toxicity. Treatment with an alcohol dehydrogenase inhibitor such as ethanol or fomepizole may be life-saving. Fifiteen mL of a 40% solution has been fatal, and as little as 10mL has caused blindness. Due to the current relative concentrations of methanol (2%) and ethanol (98%) in methylated spirits it is the ethanol which is the more toxic in acute ingestions. In Australia there is no methanol contained in methylated spirits. Methanol is metabolised by alcohol dehydrogenase to formaldehyde, which does not accumulate to a significant degree, but is metabolised to formic acid. Formic acid is metabolised more slowly and accumulates. Formic acid dissociates to formate and a hydrogen ion. The formate is metabolised to CO2 and water by a folate-dependent mechanism (Figure 1). Formic acid inhibits mitochondrial cytochrome oxidase activity, preventing oxidative metabolism and so producing "tissue hypoxia" in a manner similar to cyanide and carbon monoxide. Systemic acidosis is produced through the production of formic acid and the generatio Continue reading >>

Anion Gap

Anion Gap

Pathophysiology sample values BMP/ELECTROLYTES: Na+ = 140 Cl− = 100 BUN = 20 / Glu = 150 K+ = 4 CO2 = 22 PCr = 1.0 \ ARTERIAL BLOOD GAS: HCO3− = 24 paCO2 = 40 paO2 = 95 pH = 7.40 ALVEOLAR GAS: pACO2 = 36 pAO2 = 105 A-a g = 10 OTHER: Ca = 9.5 Mg2+ = 2.0 PO4 = 1 CK = 55 BE = −0.36 AG = 16 SERUM OSMOLARITY/RENAL: PMO = 300 PCO = 295 POG = 5 BUN:Cr = 20 URINALYSIS: UNa+ = 80 UCl− = 100 UAG = 5 FENa = 0.95 UK+ = 25 USG = 1.01 UCr = 60 UO = 800 PROTEIN/GI/LIVER FUNCTION TESTS: LDH = 100 TP = 7.6 AST = 25 TBIL = 0.7 ALP = 71 Alb = 4.0 ALT = 40 BC = 0.5 AST/ALT = 0.6 BU = 0.2 AF alb = 3.0 SAAG = 1.0 SOG = 60 CSF: CSF alb = 30 CSF glu = 60 CSF/S alb = 7.5 CSF/S glu = 0.4 The anion gap[1][2] (AG or AGAP) is a value calculated from the results of multiple individual medical lab tests. It may be reported with the results of an Electrolyte Panel, which is often performed as part of a Comprehensive Metabolic Panel.[3] The anion gap is the difference between the measured cations (positively charged ions) and the measured anions (negatively charged ions) in serum, plasma, or urine. The magnitude of this difference (i.e., "gap") in the serum is often calculated in medicine when attempting to identify the cause of metabolic acidosis, a lower than normal pH in the blood. If the gap is greater than normal, then high anion gap metabolic acidosis is diagnosed. The term "anion gap" usually implies "serum anion gap", but the urine anion gap is also a clinically useful measure.[4][5][6][7] Calculation[edit] The anion gap is a calculated measure. This means that it is not directly measured by a specific lab test; rather, it is computed with a formula that uses the results of several individual lab tests, each of which measures the concentration of a specific anion or cation. The concentr Continue reading >>

Acidosis

Acidosis

For acidosis referring to acidity of the urine, see renal tubular acidosis. "Acidemia" redirects here. It is not to be confused with Academia. Acidosis is a process causing increased acidity in the blood and other body tissues (i.e., an increased hydrogen ion concentration). If not further qualified, it usually refers to acidity of the blood plasma. The term acidemia describes the state of low blood pH, while acidosis is used to describe the processes leading to these states. Nevertheless, the terms are sometimes used interchangeably. The distinction may be relevant where a patient has factors causing both acidosis and alkalosis, wherein the relative severity of both determines whether the result is a high, low, or normal pH. Acidosis is said to occur when arterial pH falls below 7.35 (except in the fetus – see below), while its counterpart (alkalosis) occurs at a pH over 7.45. Arterial blood gas analysis and other tests are required to separate the main causes. The rate of cellular metabolic activity affects and, at the same time, is affected by the pH of the body fluids. In mammals, the normal pH of arterial blood lies between 7.35 and 7.50 depending on the species (e.g., healthy human-arterial blood pH varies between 7.35 and 7.45). Blood pH values compatible with life in mammals are limited to a pH range between 6.8 and 7.8. Changes in the pH of arterial blood (and therefore the extracellular fluid) outside this range result in irreversible cell damage.[1] Signs and symptoms[edit] General symptoms of acidosis.[2] These usually accompany symptoms of another primary defect (respiratory or metabolic). Nervous system involvement may be seen with acidosis and occurs more often with respiratory acidosis than with metabolic acidosis. Signs and symptoms that may be seen i Continue reading >>

Anion Gap

Anion Gap

The anion gap is the difference between primary measured cations (sodium Na+ and potassium K+) and the primary measured anions (chloride Cl- and bicarbonate HCO3-) in serum. This test is most commonly performed in patients who present with altered mental status, unknown exposures, acute renal failure, and acute illnesses. [1] See the Anion Gap calculator. The reference range of the anion gap is 3-11 mEq/L The normal value for the serum anion gap is 8-16 mEq/L. However, there are always unmeasurable anions, so an anion gap of less than 11 mEq/L using any of the equations listed in Description is considered normal. For the urine anion gap, the most prominently unmeasured anion is ammonia. Healthy subjects typically have a gap of 0 to slightly normal (< 10 mEq/L). A urine anion gap of more than 20 mEq/L is seen in metabolic acidosis when the kidneys are unable to excrete ammonia (such as in renal tubular acidosis). If the urine anion gap is zero or negative but the serum AG is positive, the source is most likely gastrointestinal (diarrhea or vomiting). [2] Continue reading >>

Ketosis, Cognitive Defect, Metabolic Acidosis: Causes & Diagnoses | Symptoma.com

Ketosis, Cognitive Defect, Metabolic Acidosis: Causes & Diagnoses | Symptoma.com

Causes: Metabolic Acidosis and Elevated Anion Gap (Mnemonic: "MUD PILERS") Methanol , Metformin Uremia Diabetic Ketoacidosis (DKA), Alcohol ic ketoacidosis or starvation ketosis [fpnotebook.com] Causes of metabolic acidosis There are many causes. [patient.info] Lactic Acidosis Lactic acidosis is a high anion gap metabolic acidosis due to elevated blood lactate. [merckmanuals.com] Causes: Metabolic Acidosis and Elevated Osmolal Gap Toxic Alcohol ingestion Eythylene glycol Methanol Serum K etone increase (ketosis) Alcohol ic ketoacidosis Diabetic Ketoacidosis [fpnotebook.com] Correlation between anion gap and causes of metabolic acidosis Elevated AG metabolic acidoses Lactic acidosis caused by L-lactate, due to state of hypoperfusion, carbon monoxide [patient.info] Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. [merckmanuals.com] Causes: Metabolic Acidosis and Elevated Anion Gap (Mnemonic: "MUD PILERS") Methanol , Metformin Uremia Diabetic Ketoacidosis (DKA), Alcohol ic ketoacidosis or starvation ketosis [fpnotebook.com] Causes of metabolic acidosis There are many causes. [patient.info] metabolic acidosis in Medicine metabolic acidosis n. [dictionary.reference.com] Causes: Metabolic Acidosis and Elevated Osmolal Gap Toxic Alcohol ingestion Eythylene glycol Methanol Serum K etone increase (ketosis) Alcohol ic ketoacidosis Diabetic Ketoacidosis [fpnotebook.com] Correlation between anion gap and causes of metabolic acidosis Elevated AG metabolic acidoses Lactic acidosis caused by L-lactate, due to state of hypoperfusion, carbon monoxide [patient.info] metabolic , Metabolic acidosis NOS , Metabolic Acidoses , Acidosis, Metabolic , Acidoses, Metabolic , Metabolic Acidosis , acidosis metabolic , metabolic acidosis disorder [fpnotebook. Continue reading >>

Anion Gap - Wikipedia, The Free Encyclopedia

Anion Gap - Wikipedia, The Free Encyclopedia

Discover everything Scribd has to offer, including books and audiobooks from major publishers. Anion gap - Wikipedia, the free encyclopedia saveSave Anion gap - Wikipedia, the free encyclopedia For Later Anion gap - Wikipedia, the free encyclopedia saveSave Anion gap - Wikipedia, the free encyclopedia For Later Anion gap - Wikipedia, the free encyclopedia Article Discussion Read Edit Search Navigation This article may be too technical for most readers to Main page understand. Please improve this article to make it Contents understandable to non-experts, without removing the technical Featured content details. (April 2010) Current events The anion gap is used to aid in the differential Pathophysiology sample values Although the term "anion gap" usually implies "serum Na + =140 Cl =100 BUN =20 / anion gap", the urine anion gap is also a clinically useful Interaction Glu =150 K + =4 CO 2 =22 PCr=1.0 \ Contents [hide] ARTERIAL BLOOD GAS: Community portal 1 Calculation HCO3 -=24 p a CO 2 =40 p a O 2 =95 pH=7.40 Recent changes 1.1 With potassium Contact Wikipedia 1.2 Without potassium (Daily practice) 4 Interpretation and causes Ca=9.5 Mg 2+ =2.0 PO 4 =1 What links here 4.1 High anion gap CK=55 BE =0.36 AG =16 Related changes 4.2 Normal anion gap Upload file 4.3 Low anion gap PMO = 300 PCO=295 POG =5 BUN:Cr=20 Cite this page UNa + =80 UCl =100 UAG=5 FENa =0.95 UK + =25 USG=1.01 UCr=60 UO=800 Calculation [edit] The concentrations are expressed in units of Create a book LDH =100 TP=7.6 AST=25 TBIL =0.7 milliequivalents/liter (mEq/L) or in millimoles/litre Download as PDF ALP =71 Alb =4.0 ALT=40 BC=0.5 With potassium [edit] AF alb =3.0 SAAG =1.0 SOG =60 It is calculated by subtracting the serum concentrations CSF: of chloride and bicarbonate (anions) from the CSF alb =30 CSF gl Continue reading >>

Normal Anion Gap Acidosis

Normal Anion Gap Acidosis

In renal physiology , normal anion gap acidosis, and less precisely non-anion gap acidosis, is an acidosis that is not accompanied by an abnormally increased anion gap . The most common cause of normal anion gap acidosis is diarrhea with a renal tubular acidosis being a distant second. The differential diagnosis of normal anion gap acidosis is relatively short (when compared to the differential diagnosis of acidosis): Diarrhea : due to a loss of bicarbonate. This is compensated by an increase in chloride concentration, thus leading to a normal anion gap, or hyperchloremic, metabolic acidosis. The pathophysiology of increased chloride concentration is the following: fluid secreted into the gut lumen contains higher amounts of Na+ than Cl; large losses of these fluids, particularly if volume is replaced with fluids containing equal amounts of Na+ and Cl, results in a decrease in the plasma Na+ concentration relative to the Clconcentration. This scenario can be avoided if formulations such as lactated Ringers solution are used instead of normal saline to replace GI losses. [2] Continue reading >>

Delta Ratio - Wikipedia

Delta Ratio - Wikipedia

Delta ratio is a formula that can be used to assess elevated anion gap metabolic acidosis and to evaluate whether a mixed acid base disorder ( metabolic acidosis ) is present. The anion gap (AG) is calculated first and if an anion gap is present, results in either a high anion gap metabolic acidosis (HAGMA) or a normal anion gap acidosis (NAGMA). A low anion gap is usually an oddity of measurement, rather than a clinical concern. The equation for calculating the Delta Ratio is: (AG 12) ___________ (24 - [HCO3]) [1] and reflects either an increase in the anion gap or a decrease in the bicarbonate concentration ( [HCO3] ). [2] 2. 0.4 - 0.8 due to a mixed NAGMA + HAGMA 4. >2.0 due to a mixed HAGMA + metabolic alkalosis (or pre-existing compensated respiratory acidosis) Results 2 and 4 are the ones which have mixed acid-base disorders. Results 1. and 4. are oddities, mathematically speaking: Result 1: if there is a normal anion gap acidosis, the [ AG - 12 ] part of the equation will be close to zero, the delta ratio will be close to zero and there is no mixed acid-base disorder. Your calculations can stop here. A normal anion gap acidosis (NAGMA) has more to do with a change in [Cl]) or [HCO3] concentrations. So the AG doesnt change; but to maintain electrical equilibrium, if [Cl] goes up, [HCO3] must come down. Hence, hyperchloremia always causes a metabolic acidosis as [HCO3] must fall; alternatively, if the [HCO3] rises, the [Cl] must fall. For a list of the common causes of this change in bicarbonate or chloride, see normal anion gap acidosis . Results 2-4 all involve HAGMAs. A high anion gap metabolic acidosis usually occurs because of an increase in anions. So in the equation: it is the [A] that is the cause. For a list of the common anions responsible, see high anio Continue reading >>

Normal Anion Gap Metabolic Acidosis

Normal Anion Gap Metabolic Acidosis

Home | Critical Care Compendium | Normal Anion Gap Metabolic Acidosis Normal Anion Gap Metabolic Acidosis (NAGMA) HCO3 loss and replaced with Cl- -> anion gap normal if hyponatraemia is present the plasma [Cl-] may be normal despite the presence of a normal anion gap acidosis -> this could be considered a ‘relative hyperchloraemia’. Extras – RTA, ingestion of oral acidifying salts, recovery phase of DKA loss of bicarbonate with chloride replacement -> hyperchloraemic acidosis secretions into the large and small bowel are mostly alkaline with a bicarbonate level higher than that in plasma. some typical at risk clinical situations are: external drainage of pancreatic or biliary secretions (eg fistulas) this should be easily established by history normally 85% of filtered bicarbonate is reabsorbed in the proximal tubule and the remaining 15% is reabsorbed in the rest of the tubule in patients receiving acetazolamide (or other carbonic anhydrase inhibitors), proximal reabsorption of bicarbonate is decreased resulting in increased distal delivery and HCO3- appears in urine this results in a hyperchloraemic metabolic acidosis and is essentially a form of proximal renal tubular acidosis but is usually not classified as such. hyperchloraemic metabolic acidosis commonly develops during therapy of diabetic ketoacidosis with normal saline oral administration of CaCl2 or NH4Cl is equivalent to giving an acid load both of these salts are used in acid loading tests for the diagnosis of renal tubular acidosis CaCl2 reacts with bicarbonate in the small bowel resulting in the production of insoluble CaCO3 and H+ the hepatic metabolism of NH4+ to urea results in an equivalent production of H+ REASONS WHY ANION GAP MAY BE NORMAL DESPITE A ‘HIGH ANION GAP METABOLIC ACIDOSIS’ 1. Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic Acidosis Definition Metabolic acidosis is a pH imbalance in which the body has accumulated too much acid and does not have enough bicarbonate to effectively neutralize the effects of the acid. Description Metabolic acidosis, as a disruption of the body's acid/base balance, can be a mild symptom brought on by a lack of insulin, a starvation diet, or a gastrointestinal disorder like vomiting and diarrhea. Metabolic acidosis can indicate a more serious problem with a major organ like the liver, heart, or kidneys. It can also be one of the first signs of drug overdose or poisoning. Causes and symptoms Metabolic acidosis occurs when the body has more acid than base in it. Chemists use the term "pH" to describe how acidic or basic a substance is. Based on a scale of 14, a pH of 7.0 is neutral. A pH below 7.0 is an acid; the lower the number, the stronger the acid. A pH above 7.0 is a base; the higher the number, the stronger the base. Blood pH is slightly basic (alkaline), with a normal range of 7.36-7.44. Acid is a natural by-product of the breakdown of fats and other processes in the body; however, in some conditions, the body does not have enough bicarbonate, an acid neutralizer, to balance the acids produced. This can occur when the body uses fats for energy instead of carbohydrates. Conditions where metabolic acidosis can occur include chronic alcoholism, malnutrition, and diabetic ketoacidosis. Consuming a diet low in carbohydrates and high in fats can also produce metabolic acidosis. The disorder may also be a symptom of another condition like kidney failure, liver failure, or severe diarrhea. The build up of lactic acid in the blood due to such conditions as heart failure, shock, or cancer, induces metabolic acidosis. Some poisonings and overdoses (aspirin, Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia. Alcoholic ketoacidosis causes nausea, vomiting, and abdominal pain. Diagnosis is by history and findings of ketoacidosis without hyperglycemia. Treatment is IV saline solution and dextrose infusion. Alcoholic ketoacidosis is attributed to the combined effects of alcohol and starvation on glucose metabolism. Alcohol diminishes hepatic gluconeogenesis and leads to decreased insulin secretion, increased lipolysis, impaired fatty acid oxidation, and subsequent ketogenesis, causing an elevated anion gap metabolic acidosis. Counter-regulatory hormones are increased and may further inhibit insulin secretion. Plasma glucose levels are usually low or normal, but mild hyperglycemia sometimes occurs. Diagnosis requires a high index of suspicion; similar symptoms in an alcoholic patient may result from acute pancreatitis, methanol or ethylene glycol poisoning, or diabetic ketoacidosis (DKA). In patients suspected of having alcoholic ketoacidosis, serum electrolytes (including magnesium), BUN and creatinine, glucose, ketones, amylase, lipase, and plasma osmolality should be measured. Urine should be tested for ketones. Patients who appear significantly ill and those with positive ketones should have arterial blood gas and serum lactate measurement. The absence of hyperglycemia makes DKA improbable. Those with mild hyperglycemia may have underlying diabetes mellitus, which may be recognized by elevated levels of glycosylated Hb (HbA1c). Typical laboratory findings include a high anion gap metabolic acidosis, ketonemia, and low levels of potassium, magnesium, and phosphorus. Detection of acidosis may be com Continue reading >>

Acid-base Balance

Acid-base Balance

Acid-base balance is critical when testing feline biochemistry to assess homeostasis. Acid-base balance is important for maintaining the narrow pH range that is required for various enzyme systems to function optimally in the body. Normal blood pH ranges from 7.3-7.4.3 Decreased pH is termed acidemia and is caused by an increase in the concentration of hydrogen ions ([H+]). Increased blood pH is termed alkalemia and is caused by a decrease in the [H+]. The buffer systems that maintain this pH balance are bicarbonate, phosphates, and proteins.(4) Bicarbonate is the most important extracellular buffer, while phosphates and proteins contribute mostly to intracellular acid-base balance.(2) The bicarbonate system is the only buffer measured for the calculation of acid-base status in patients and is represented by the equilibrium equation: CO2 + H2O <—> H2CO3 <—> H+ + HCO3-. This equation allows one to visualize what effects the addition of carbon dioxide (CO2) or bicarbonate (HCO3-) will have on the buffer system and the blood pH. Addition of CO2 to the system will cause the equation to shift to the right, increasing the [H+] and, therefore, lowering the pH. Addition of HCO3- to the system will cause the equation to shift to the left, lowering the [H+] and increasing the pH. Another way to conceptualize this information is to simply think of CO2 as an acid and HCO3- as a base. If CO2 is increased it will tend to cause acidemia. If HCO3- is increased, then alkalemia is the expected result. In addition to buffers, the lungs and kidneys play a major role in acid-base homeostasis. The lungs function in ventilation and they are responsible for regulating the amount of CO2 present in plasma. The kidneys are responsible for controlling the amount of HCO3- in the blood by resorb Continue reading >>

More in ketosis