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Metabolic Acidosis Pathophysiology Ppt

Metabolic Acidosis: Pathophysiology, Diagnosis And Management.

Metabolic Acidosis: Pathophysiology, Diagnosis And Management.

Nat Rev Nephrol. 2010 May;6(5):274-85. doi: 10.1038/nrneph.2010.33. Epub 2010 Mar 23. Metabolic acidosis: pathophysiology, diagnosis and management. Division of Nephrology, Veterans Administration Greater Los Angeles Healthcare System, 11301 Wilshire Boulevard, Los Angeles, CA 90073, USA. Metabolic acidosis is characterized by a primary reduction in serum bicarbonate (HCO(3)(-)) concentration, a secondary decrease in the arterial partial pressure of carbon dioxide (PaCO(2)) of approximately 1 mmHg for every 1 mmol/l fall in serum HCO(3)(-) concentration, and a reduction in blood pH. Acute forms (lasting minutes to several days) and chronic forms (lasting weeks to years) of the disorder can occur, for which the underlying cause/s and resulting adverse effects may differ. Acute forms of metabolic acidosis most frequently result from the overproduction of organic acids such as ketoacids or lactic acid; by contrast, chronic metabolic acidosis often reflects bicarbonate wasting and/or impaired renal acidification. The calculation of the serum anion gap, calculated as [Na(+)] - ([HCO(3)(-)] + [Cl(-)]), aids diagnosis by classifying the disorders into categories of normal (hyperchloremic) anion gap or elevated anion gap. These categories can overlap, however. Adverse effects of acute metabolic acidosis primarily include decreased cardiac output, arterial dilatation with hypotension, altered oxygen delivery, decreased ATP production, predisposition to arrhythmias, and impairment of the immune response. The main adverse effects of chronic metabolic acidosis are increased muscle degradation and abnormal bone metabolism. Using base to treat acute metabolic acidosis is controversial because of a lack of definitive benefit and because of potential complications. By contrast, the ad Continue reading >>

Mala: Metformin-associated Lactic Acidosis

Mala: Metformin-associated Lactic Acidosis

By Charles W. O’Connell, MD Introduction Metformin is a first-line agent for type 2 diabetes mellitus often used as monotherapy or in combination with oral diabetic medications. It is a member of the biguanide class and its main intended effect is expressed by the inhibition of hepatic gluconeogenesis. In addition, metformin increases insulin sensitivity, enhances peripheral glucose utilization and decreases glucose uptake in the gastrointestinal tract. Phenformin, a previously used biguanide, as withdrawn from the market in the 1970’s due its association with numerous cases of lactic acidosis. Metformin is currently used extensively in the management of diabetes and is the most commonly prescribed biguanide worldwide. The therapeutic dosage of metformin ranges from 850 mg to a maximum of 3000 mg daily and is typically divided into twice daily dosing. It is primarily used in the treatment of diabetes but has been used in other conditions associated with insulin resistance such as polycystic ovarian syndrome. MALA is a rare but well reported event that occurs with both therapeutic use and overdose states. Case presentation A 22-year-old female presents to the Emergency Department after being found alongside a suicide note by her family. She was thought to have taken an unknown, but large amount of her husband’s metformin. She arrives at the ED nearly 10 hours after ingestion. She was agitated, but conversant. She reports having nausea and vague feelings of being unwell and is very distraught over the state of her critically ill husband. She has some self-inflicted superficial lacerations over her left anterior forearm. Her vital assigns upon arrival were: T 98.9 degrees Fahrenheit, HR initially 140 bpm which improved to 110 bpm soon after arrival, BP 100/50, RR 22, Continue reading >>

New Findings On The Pathogenesis Of Distal Renal Tubular Acidosis

New Findings On The Pathogenesis Of Distal Renal Tubular Acidosis

The Kidney in Genetic and Rare Diseases: Review New Findings on the Pathogenesis of Distal Renal Tubular Acidosis Trepiccione F.a Prosperi F.a, b de la Motte L.R.a, b Hbner C.A.c Chambrey R.d Eladari D.e Capasso G.a, b aDepartment of Cardiothoracic and Respiratory Science, University of Campania Luigi Vanvitelli, Naples, and bBiogem S.c.a.r.l., Research Institute Gaetano Salvatore, Ariano Irpino, Italy; cInstitute of Human Genetics, Jena University Hospital, Friedrich Schiller University, Jena, Germany; dInserm U1188, Diabte athrothrombose Thrapies Runion Ocan Indien (DTROI), Universit de La Runion, and eService d'Explorations Fonctionnelles Rnales, Hpital Felix Guyon, CHU de la Runion, Saint-Denis, Ile de la Runion, France Department of Cardiothoracic and Respiratory Science University of Campania Luigi Vanvitelli E-Mail [email protected] Background: Distal renal tubular acidosis (dRTA) is characterized by an impairment of the urinary acidification process in the distal nephron. Complete or incomplete metabolic acidosis coupled with inappropriately alkaline urine are the hallmarks of this condition. Genetic forms of dRTA are caused by loss of function mutations of either SLC4A1, encoding the AE1 anion exchanger, or ATP6V1B1 and ATP6V0A4, encoding for the B1 and a4 subunits of the vH+ATPase, respectively. These genes are crucial for the function of A-type intercalated cells (A-IC) of the distal nephron. Summary: Alterations of acid-base homeostasis are variably associated with hypokalemia, hypercalciuria, nephrocalcinosis or nephrolithiasis, and a salt-losing phenotype. Here we report the diagnostic test and the underlying physiopathological mechanisms. The molecular mechanisms identified so far can explain the defect in acid secretion, but do not ex Continue reading >>

Metabolic Acidosis Treatment & Management: Approach Considerations, Type 1 Renal Tubular Acidosis, Type 2 Renal Tubular Acidosis

Metabolic Acidosis Treatment & Management: Approach Considerations, Type 1 Renal Tubular Acidosis, Type 2 Renal Tubular Acidosis

Metabolic AcidosisTreatment & Management Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FASN more... 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 whi Continue reading >>

Metabolic Acidosis Nursing Management And Interventions - Nurseslabs

Metabolic Acidosis Nursing Management And Interventions - Nurseslabs

Metabolic Acidosisis an acid-base imbalance resulting from excessive absorption or retention of acid or excessive excretion of bicarbonate produced by an underlying pathologic disorder. Symptoms result from the bodys attempts to correct the acidotic condition through compensatory mechanisms in the lungs , kidneys and cells. Metabolic acidosis is characterized by normal or high anion gap situations. If the primary problem is direct loss of bicarbonate, gain of chloride, or decreased ammonia production, the anion gap is within normal limits. If the primary problem is the accumulation of organic anions (such as ketones or lactic acid), the condition is known as high anion gap acidosis. Compensatory mechanisms to correct this imbalance include an increase in respirations to blow off excess CO2, an increase in ammonia formation, and acid excretion (H+) by the kidneys, with retention of bicarbonate and sodium . High anion gap acidosis occurs in diabetic ketoacidosis ; severe malnutrition or starvation, alcoholic lactic acidosis; renal failure; high-fat, low-carbohydrate diets/lipid administration; poisoning, e.g., salicylate intoxication (after initial stage); paraldehyde intoxication; and drug therapy, e.g., acetazolamide (Diamox), NH4Cl. Normal anion gap acidosis is associated with loss of bicarbonate form the body, as may occur in renal tubular acidosis, hyperalimentation, vomiting/ diarrhea , small-bowel/pancreatic fistulas, and ileostomy and use of IV sodium chloride in presence of preexisting kidney dysfunction, acidifying drugs (e.g., ammonium chloride). This condition does not occur in isolation but rather is a complication of a broader problem that may require inpatient care in a medical-surgical or subacute unit. Use of carbonic anhydrase inhibitors or anion-exchan Continue reading >>

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Management Of Metabolic Acidosis

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Management Of Metabolic Acidosis

Recommendations for the treatment of acute metabolic acidosis Gunnerson, K. J., Saul, M., He, S. & Kellum, J. Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients. Crit. Care Med. 10, R22-R32 (2006). Eustace, J. A., Astor, B., Muntner, P M., Ikizler, T. A. & Coresh, J. Prevalence of acidosis and inflammation and their association with low serum albumin in chronic kidney disease. Kidney Int. 65, 1031-1040 (2004). Kraut, J. A. & Kurtz, I. Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment. Am. J. Kidney Dis. 45, 978-993 (2005). Kalantar-Zadeh, K., Mehrotra, R., Fouque, D. & Kopple, J. D. Metabolic acidosis and malnutrition-inflammation complex syndrome in chronic renal failure. Semin. Dial. 17, 455-465 (2004). Kraut, J. A. & Kurtz, I. Controversies in the treatment of acute metabolic acidosis. NephSAP 5, 1-9 (2006). Cohen, R. M., Feldman, G. M. & Fernandez, P C. The balance of acid base and charge in health and disease. Kidney Int. 52, 287-293 (1997). Rodriguez-Soriano, J. & Vallo, A. Renal tubular acidosis. Pediatr. Nephrol. 4, 268-275 (1990). Wagner, C. A., Devuyst, O., Bourgeois, S. & Mohebbi, N. Regulated acid-base transport in the collecting duct. Pflugers Arch. 458, 137-156 (2009). Boron, W. F. Acid base transport by the renal proximal tubule. J. Am. Soc. Nephrol. 17, 2368-2382 (2006). Igarashi, T., Sekine, T. & Watanabe, H. Molecular basis of proximal renal tubular acidosis. J. Nephrol. 15, S135-S141 (2002). Sly, W. S., Sato, S. & Zhu, X. L. Evaluation of carbonic anhydrase isozymes in disorders involving osteopetrosis and/or renal tubular acidosis. Clin. Biochem. 24, 311-318 (1991). Dinour, D. et al. A novel missense mutation in the sodium bicarbonate cotransporter (NBCe1/ SLC4A4) Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Professor of Pediatric Endocrinology University of Khartoum, Sudan Introduction DKA is a serious acute complications of Diabetes Mellitus. It carries significant risk of death and/or morbidity especially with delayed treatment. The prognosis of DKA is worse in the extremes of age, with a mortality rates of 5-10%. With the new advances of therapy, DKA mortality decreases to > 2%. Before discovery and use of Insulin (1922) the mortality was 100%. Epidemiology DKA is reported in 2-5% of known type 1 diabetic patients in industrialized countries, while it occurs in 35-40% of such patients in Africa. DKA at the time of first diagnosis of diabetes mellitus is reported in only 2-3% in western Europe, but is seen in 95% of diabetic children in Sudan. Similar results were reported from other African countries . Consequences The latter observation is annoying because it implies the following: The late diagnosis of type 1 diabetes in many developing countries particularly in Africa. The late presentation of DKA, which is associated with risk of morbidity & mortality Death of young children with DKA undiagnosed or wrongly diagnosed as malaria or meningitis. Pathophysiology Secondary to insulin deficiency, and the action of counter-regulatory hormones, blood glucose increases leading to hyperglycemia and glucosuria. Glucosuria causes an osmotic diuresis, leading to water & Na loss. In the absence of insulin activity the body fails to utilize glucose as fuel and uses fats instead. This leads to ketosis. Pathophysiology/2 The excess of ketone bodies will cause metabolic acidosis, the later is also aggravated by Lactic acidosis caused by dehydration & poor tissue perfusion. Vomiting due to an ileus, plus increased insensible water losses due to tachypnea will worsen the state of dehydr Continue reading >>

Traumas Lethal Triad Of Hypothermia, Acidosis & Coagulopathy Create A Deadly Cycle For Trauma Patients

Traumas Lethal Triad Of Hypothermia, Acidosis & Coagulopathy Create A Deadly Cycle For Trauma Patients

Traumas Lethal Triad of Hypothermia, Acidosis & Coagulopathy Create a Deadly Cycle for Trauma Patients When patients are resuscitated with a fluid that doesn't contain the same clotting factors as blood, dilutional coagulopathy can occur. Photo courtesy Edmonton EMS Listthe individual components of the lethal triad of trauma. Understandthe pathophysiology that makes the lethal triad a deadly self-propogating cycle in critically ill trauma patients. Learnsimple interventions EMS providers can perform to help prevent or slow the rapid progression of the lethal triad. Acidosis:Lower than normal pH due to increased hydrogen ion concentration. Coagulation system:A temperature- and pH-dependent series of complex enzymatic reactions that result in the formation of blood clots to stop both internal and external hemorrhage. Coagulopathy:Any disorder of the blood that makes it difficult for blood to coagulate. Hypothermia:Lowered body core temperature. Lethal triad:A combination of acidosis, coagulopathy and hypothermia that usually leads to death in a patient experiencing trauma. Its 11 p.m. on a Saturday night when youre dispatched to a local nightclub for reports of a young male whos suffered multiple gunshot wounds. En route, police notify you the scene is safe and theres a single patient bleeding profusely from multiple extremity wounds. On arrival you find a 25-year-old male lying on the street in a rapidly expanding pool of blood. Hes nearly unconscious but breathing spontaneously. His skin is cool, moist and pale. His pulse is rapid and barely palpable. As you and your partner begin your rapid trauma assessment, obtain vital signs, and prepare for rapid packaging and transport to the trauma center 20 minutes away, you know this young man is on the brink of death. Despite Continue reading >>

Grain Overload In Ruminants

Grain Overload In Ruminants

(Lactic acidosis, Carbohydrate engorgement, Rumenitis) By Peter D. Constable, BVSc (Hons), MS, PhD, DACVIM, Dean, College of Veterinary Medicine, University of Illinois Grain overload is an acute disease of ruminants that is characterized by rumen hypomotility to atony, dehydration, acidemia, diarrhea, depression, incoordination, collapse, and in severe cases, death. The disease is most common in cattle that accidentally gain access to large quantities of readily digestible carbohydrates, particularly grain. Grain overload also is common in feedlot cattle when they are introduced to heavy grain diets too quickly. Wheat, barley, and corn are the most readily digestible grains; oats are less digestible. Less common causes include engorgement with apples, grapes, bread, batters dough, sugar beets, potatoes, mangels, or sour wet brewers grain that was incompletely fermented in the brewery. The amount of feed required to produce acute illness depends on the kind of grain, previous experience of the animal with that grain, the nutritional status and condition of the animal, and the nature of the ruminal microflora. Adult cattle accustomed to heavy grain diets may consume 3045 lb (1520 kg) of grain and develop only moderate illness, whereas others may become acutely ill and die after eating 20 lb (10 kg) of grain. Ingestion of toxic amounts of highly fermentable carbohydrates is followed within 26 hr by a change in the microbial population in the rumen. The number of gram-positive bacteria (such as Streptococcus bovis) increases markedly, which results in the production of large quantities of lactic acid. The rumen pH falls to 5, which destroys protozoa, cellulolytic organisms, and lactate-utilizing organisms, and impairs rumen motility. The low pH allows the lactobacilli to Continue reading >>

Blood Gas Analysis--insight Into The Acid-base Status Of The Patient

Blood Gas Analysis--insight Into The Acid-base Status Of The Patient

Acid-Base Physiology Buffers H+ A- HCO3- CO2 Buffers H+ A- CO2 Cells Blood Kidney Lungs Fluids, Electrolytes, and Acid-Base Status in Critical Illness Blood Gas Analysis--Insight into the Acid-Base status of the Patient The blood gas consists of pH-negative log of the Hydrogen ion concentration: -log[H+]. (also, pH=pK+log [HCO3]/ 0.03 x pCO2). The pH is always a product of two components, respiratory and metabolic, and the metabolic component is judged, calculated, or computed by allowing for the effect of the pCO2, ie, any change in the pH unexplained by the pCO2 indicates a metabolic abnormality. CO +H 0ºº H CO ººHCO + H2 2 2 3 3 - + CO2 and water form carbonic acid or H2CO3, which is in equilibrium with bicarbonate (HCO3-)and hydrogen ions (H+). A change in the concentration of the reactants on either side of the equation affects the subsequent direction of the reaction. For example, an increase in CO2 will result in increased carbonic acid formation (H2CO3) which leads to an increase in both HCO3- and H+ (\pH). Normally, at pH 7.4, a ratio of one part carbonic acid to twenty parts bicarbonate is present in the extracellular fluid [HCO3-/H2CO3]=20. A change in the ratio will affect the pH of the fluid. If both components change (ie, with chronic compensation), the pH may be normal, but the other components will not. pCO -partial pressure of carbon dioxide. Hypoventilation or hyperventilation (ie, minute2 ventilation--tidal volume x respitatory rate--imperfectly matched to physiologic demands) will lead to elevation or depression, respectively, in the pCO2. V/Q (ventilation/perfusion) mismatch does not usually lead to abnormalities in PCO2 because of the linear nature of the CO2 elimination curve (ie, good lung units can make up for bad lung units). Diffus Continue reading >>

Chapter 47. Acidosis And Alkalosis

Chapter 47. Acidosis And Alkalosis

DuBose TD, Jr.. DuBose T.D., Jr. DuBose, Thomas D., Jr.Chapter 47. Acidosis and Alkalosis. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J. Longo D.L., Fauci A.S., Kasper D.L., Hauser S.L., Jameson J, Loscalzo J Eds. Dan L. Longo, et al.eds. Harrison's Principles of Internal Medicine, 18e New York, NY: McGraw-Hill; 2012. Accessed April 22, 2018. DuBose TD, Jr.. DuBose T.D., Jr. DuBose, Thomas D., Jr.. "Chapter 47. Acidosis and Alkalosis." Harrison's Principles of Internal Medicine, 18e Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J. Longo D.L., Fauci A.S., Kasper D.L., Hauser S.L., Jameson J, Loscalzo J Eds. Dan L. Longo, et al. New York, NY: McGraw-Hill, 2012, Systemic arterial pH is maintained between 7.35 and 7.45 by extracellular and intracellular chemical buffering together with respiratory and renal regulatory mechanisms. The control of arterial CO2 tension (Paco2) by the central nervous system (CNS) and respiratory systems and the control of the plasma bicarbonate by the kidneys stabilize the arterial pH by excretion or retention of acid or alkali. The metabolic and respiratory components that regulate systemic pH are described by the Henderson-Hasselbalch equation: Under most circumstances, CO2 production and excretion are matched, and the usual steady-state Paco2 is maintained at 40 mmHg. Underexcretion of CO2 produces hypercapnia, and overexcretion causes hypocapnia. Nevertheless, production and excretion are again matched at a new steady-state Paco2. Therefore, the Paco2 is regulated primarily by neural respiratory factors and is not subject to regulation by the rate of CO2 production. Hypercapnia is usually the result of hypoventilation rather than of increased CO2 production. Increases or decreases in Paco2 represent de Continue reading >>

Chapter 47. Acidosis And Alkalosis

Chapter 47. Acidosis And Alkalosis

DuBose TD, Jr.. DuBose T.D., Jr. DuBose, Thomas D., Jr.Chapter 47. Acidosis and Alkalosis. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J. Longo D.L., Fauci A.S., Kasper D.L., Hauser S.L., Jameson J, Loscalzo J Eds. Dan L. Longo, et al.eds. Harrison's Principles of Internal Medicine, 18e New York, NY: McGraw-Hill; 2012. Accessed April 24, 2018. DuBose TD, Jr.. DuBose T.D., Jr. DuBose, Thomas D., Jr.. "Chapter 47. Acidosis and Alkalosis." Harrison's Principles of Internal Medicine, 18e Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J. Longo D.L., Fauci A.S., Kasper D.L., Hauser S.L., Jameson J, Loscalzo J Eds. Dan L. Longo, et al. New York, NY: McGraw-Hill, 2012, Systemic arterial pH is maintained between 7.35 and 7.45 by extracellular and intracellular chemical buffering together with respiratory and renal regulatory mechanisms. The control of arterial CO2 tension (Paco2) by the central nervous system (CNS) and respiratory systems and the control of the plasma bicarbonate by the kidneys stabilize the arterial pH by excretion or retention of acid or alkali. The metabolic and respiratory components that regulate systemic pH are described by the Henderson-Hasselbalch equation: Under most circumstances, CO2 production and excretion are matched, and the usual steady-state Paco2 is maintained at 40 mmHg. Underexcretion of CO2 produces hypercapnia, and overexcretion causes hypocapnia. Nevertheless, production and excretion are again matched at a new steady-state Paco2. Therefore, the Paco2 is regulated primarily by neural respiratory factors and is not subject to regulation by the rate of CO2 production. Hypercapnia is usually the result of hypoventilation rather than of increased CO2 production. Increases or decreases in Paco2 represent de Continue reading >>

Metabolic Acidosis |authorstream

Metabolic Acidosis |authorstream

Automatically changes to Flash or non-Flash embed The presentation is successfully added In Your Favorites . This Presentation is Public Favorites: ynm DDUH NEW DELHI 64 1 ACID - BASE BALANCE By Dr Y.N MAURYA M.B.B.S, D.C.H Medical Officer Deen Dayal Upadhyay Hospital Govt. of NCT New Delhi- 64 ynm DDUH NEW DELHI 64 2 SOME NORMAL VALUES pH --- 7.35-7.45HCO3 --- 22-26 mmol/LPaCO2 --- 35-45 mmHgPaO2 --- 60-100 mmHgALBUMIN-- 45.5 g/dlNa+ --- 135-145 mmol/LK+ --- 3.5-5.5 mmol/LCa+2 --- 1.12-1.23 mmol/LCl --- 98-106 mmol/L[H+] at pH 7.4 --- 40 nmol/L ynm DDUH NEW DELHI 64 3 Why pH 7.357.45 is necessary ? FOR OPTIMAL FUNCTIONING OF CELLULAR ENZYMES & METABOLIC PROCESSES : ynm DDUH NEW DELHI 64 4 FOR OPTIMAL FUNCTIONING OF CELLULAR ENZYMES & METABOLIC PROCESSES WHICH pH SHOULD BE MAINTAINED ? : ynm DDUH NEW DELHI 64 5 WHICH pH SHOULD BE MAINTAINED ? INTRACELLULAR OR EXTRACELLULAR INTRACELLULAR pH SHOULD BE MAINTAINED : ynm DDUH NEW DELHI 64 6 INTRACELLULAR pH SHOULD BE MAINTAINED IS IT INTRACELLULAR pH WHICH MEASURED NORMALY ? : ynm DDUH NEW DELHI 64 7 IS IT INTRACELLULAR pH WHICH MEASURED NORMALY ? NORMALY MEASURED pH IS EXTRACELLULAR pHBECAUSE INTRACELLULAR pH PARALLELS EXTRACELLULAR pH & LATER IS EASY,SO IT IS EXTRACELLULAR pH WHICH IS NORMALY MEASURED NORMAL PHYSIOLOGY OF ACID- BASE BALANCE : ynm DDUH NEW DELHI 64 8 NORMAL PHYSIOLOGY OF ACID- BASE BALANCE MAINTAINENCE OF EXTRACELLULAR pH & BUFFER : ynm DDUH NEW DELHI 64 9 MAINTAINENCE OF EXTRACELLULAR pH & BUFFER WHAT IS BUFFER ? . SUBSTANCES THAT ATTENUATE CHANGE IN pH.THESE ARE WEAK ACIDS OR WEAK BASES. ARE 50% DISSOCIATED AT IT'S pK (diss. Constant)BEST BUFFERS HAVE pK CLOSE TO 7.4 ynm DDUH NEW DELHI 64 10 IMPORTANT BUFFERS ? BICARBONATE BUFFER H++ HCO3 == H2O+ CO2 ( pK 6.1 ) ? NON-BICARBONATE BUFFERS 1. ALBUMIN ( PK 6 Continue reading >>

Metformin-related Lactic Acidosis: Case Report - Sciencedirect

Metformin-related Lactic Acidosis: Case Report - Sciencedirect

Open Access funded by Sociedad Colombiana de Anestesiologa y Reanimacin Lactic acidosis is defined as the presence of pH <7.35, blood lactate >2.0mmol/L and PaCO2 <42mmHg. However, the definition of severe lactic acidosis is controversial. The primary cause of severe lactic acidosis is shock. Although rare, metformin-related lactic acidosis is associated with a mortality as high as 50%. The treatment for metabolic acidosis, including lactic acidosis, may be specific or general, using sodium bicarbonate, trihydroxyaminomethane, carbicarb or continuous haemodiafiltration. The successful treatment of lactic acidosis depends on the control of the aetiological source. Intermittent or continuous renal replacement therapy is perfectly justified, shock being the argument for deciding which modality to use. We report a case of a male patient presenting with metformin poisoning as a result of attempted suicide, who developed lactic acidosis and multiple organ failure. The critical success factor was treatment with continuous haemodiafiltration. Definimos acidosis lctica en presencia de pH <7.35, lactato en sangre >2.0mmol/L y PaCO2 <42mmHg. Por otro lado, la definicin de acidosis lctica grave es controvertida. La causa principal de acidosis lctica grave es el estado de choque. La acidosis lctica por metformina es rara pero alcanza mortalidad del 50%. La acidosis metablica incluyendo a la acidosis lctica puede recibir tratamiento especfico o tratamiento general con bicarbonato de sodio, trihidroxiaminometano, carbicarb o hemodiafiltracin continua. El xito del tratamiento de la acidosis lctica yace en el control de la fuente etiolgica; la terapia de reemplazo renal intermitente o continua est perfectamente justificada, donde el argumento para decidir cul utilizar ser el estado de Continue reading >>

Transient Perioperative Metabolic Acidosis In A Patient With Ileal Bladder Augmentation | Anesthesiology | Asa Publications

Transient Perioperative Metabolic Acidosis In A Patient With Ileal Bladder Augmentation | Anesthesiology | Asa Publications

Transient Perioperative Metabolic Acidosis in a Patient with Ileal Bladder Augmentation (Azzam) Associate Professor of Anesthesiology and Pediatrics. (Steinhardt) Associate Professor of Surgery and Pediatrics. (Tracy, Gabriel) Associate Professor of Orthopedics. Received from the Cardinal Glennon Children's Hospital, St. Louis University, St. Louis, Missouri. Submitted for publication October 27, 1994. Accepted for publication February 17, 1995. Address reprint requests to Dr. Azzam: St. Louis University Hospital, 3635 Vista Avenue, St. Louis, Missouri 63110. Transient Perioperative Metabolic Acidosis in a Patient with Ileal Bladder Augmentation Anesthesiology 7 1995, Vol.83, 198-200.. doi: Anesthesiology 7 1995, Vol.83, 198-200.. doi: Farid J. Azzam, George F. Steinhardt, Thomas F. Jr. Tracy, Keith R. Gabriel; Transient Perioperative Metabolic Acidosis in a Patient with Ileal Bladder Augmentation. Anesthesiology 1995;83(1):198-200.. 2018 American Society of Anesthesiologists Transient Perioperative Metabolic Acidosis in a Patient with Ileal Bladder Augmentation You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account Key words: Acid-base equilibrium, acidosis: metabolic, Bladder. A poorly compliant, small-capacity bladder sometimes is seen in pediatric patients with myelomeningocele and other clinical entities. [1] Bladder augmentation with an intestinal segment provides the low-pressure reservoir required to preserve renal function and allow for urinary continence. [2] Metabolic complications of this procedure are well described [3] and include hyperchloremic acidosis, decrease in serum bicarbonate, and increase in serum phosphate and sulfate levels, leading to osteomalac Continue reading >>

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