http:\/\/www.acidbase.org\/<\/a> for analyzer<\/p>\n http:\/\/www.anaesthesiamcq.com\/AcidBaseBook\/ABindex.php<\/a> incredible online text<\/p>\n My Acid\/Base Sheet<\/a><\/p>\n Sodium Bicarb Review<\/a><\/p>\n Pharm induced Acidosis<\/a><\/p>\n Great Lactate Review<\/a><\/p>\n Kerry Bradshaw’s amazing Online Text<\/a><\/p>\n NEJM 1998;338(1):26<\/a><\/p>\n NEJM 1998;338(2):107<\/a><\/p>\n Quantitative Approach: (Crit Care 2005;9(2):204) and anaesthesia 2002;57(4):348<\/a><\/p>\n Anaesthesia 2002;57(4):348 Acid-\u0080\u0099base physiology: the \u009ctraditional and the \u009cmodern approaches<\/p>\n <\/p>\n albumin (g\/L) x (0.123 x pH – 0.631)<\/p>\n phosphate (mg\/dL) x (0.309 x pH – 0.469)<\/p>\n <\/p>\n <\/p>\n bicarb is only an effective buffer at pH<\/p>\n at this pH, give 50% of bicarb deficit<\/p>\n HCO3 deficit=0.6 x wt (kg) x (15-current HCO3)<\/p>\n <\/p>\n HCl Infusions<\/p>\n calculate H deficit<\/p>\n H (meq) deficit=0.5 x wt (kg) x (measured HCO3 – desired HCO3)<\/p>\n volume of 0.1N HCl (L) = H deficit\/100<\/p>\n set desired at halfway between actual and normal<\/p>\n 0.1N contains 100 mEq of H+ per liter<\/p>\n must go in central vein<\/p>\n infusion rate should not exceed 0.2 mEq\/kg\/hour<\/p>\n <\/p>\n <\/p>\n Corrected Aa Gradient=10+Age\/10<\/p>\n <\/p>\n Metabolic Acidosis <\/strong><\/p>\n PCO2=(1.5xBicarb) + 8 (+-2)<\/p>\n Metabolic Alkalosis <\/strong><\/p>\n PCO2=(0.7xBicarb) + 21 (+-1.5)<\/p>\n Respiratory Alkalosis<\/strong><\/p>\n Acute Bicarb=((CO2-40)\/10) + 24<\/p>\n Chronic Bicarb=((CO2-40)\/3) + 24<\/p>\n Respiratory Acidosis<\/strong><\/p>\n Acute Bicarb=((40-CO2)\/5) + 24<\/p>\n Chronic Bicarb=((40-CO2)\/2) + 24<\/p>\n <\/p>\n Normal Anion Gap=2 (Albumin) + 0.5 (Phosphate)<\/p>\n impairs cardiac contractility<\/p>\n arterial dilation, venous constriction<\/p>\n hyperventilation<\/p>\n inhibits anaerobic metabolism<\/p>\n hyperkalemia<\/p>\n sympathomimetic release, but attenuates the response to catecholamines (consider in b-agonists in asthmatics)<\/p>\n decreases the uptake of glucose into cells and induces insulin resistance<\/p>\n <\/p>\n The body will buffer any acid load with proteins, Hb, and creatinine.\u00a0 If the bicarb drops, it is b\/c these buffers have been overwhelmed.<\/p>\n <\/p>\n In disease states where tissue hypoxia causes the acidosis, exogenous bicarb administration is actually harmful, but if tissue hypoxia is not present, bicarb can be beneficial.<\/p>\n Bicarb can be harmful in 5 ways:<\/strong><\/p>\n <\/p>\n increased CO2 not due to pulmonary dysfunction, so the PaCO2 will remain normal, but the mixed venous will not be.\u00a0 ABGs are poorly representative of tissue acid\/base status or oxygenation.\u00a0 Central venous or mixed venous (pulmonary artery) are much more representative.<\/p>\n <\/p>\n in this state the body has 400-500 mmol of available bicarb precursor in the form of lactate and ketoacid anions.\u00a0 The addition of exogenous bicarb does not help, what helps is reversal of the process of ketosis with insulin allowing the liver to produce bicarb.<\/p>\n <\/p>\n Severe acidemia will be associated with bicarb of<\/p>\n In keto or lactic acidosis, treat the underlying disorder because endogenous anions will be converted back to bicarb<\/p>\n In hyperchloremic, patient needs bicarb<\/p>\n <\/p>\n Alkalizing salts like sodium lactate, citrate, or acetate depend on oxidation of salts to bicarb<\/p>\n <\/p>\n Give Bicarb to get pH to 7.2, so bicarb must be increased to between 8 and 10<\/p>\n Consider bicarb space to be 50% of body weight as starting point<\/p>\n so give 8-Bicarb * kg * 0.5=mmol of bicarb needed<\/p>\n Bicarb normally comes as a 1N solution (1 mmol per cc)<\/p>\n Remember admin of bicarb increases CO2 so only give if intubated or patient has compensatory reserve to blow off excess<\/p>\n <\/p>\n <\/p>\n Best Review of Lactate<\/a><\/p>\n Elevated lactate may be from alcohol alone (Am Surg. 2011 Dec;77(12):1576-9.)<\/p>\n Most pathways to excess lactate are from decreased elimination as opposed to solely increased production<\/p>\n <\/p>\n 1\/2 life of lactate is 3 hours<\/p>\n <\/p>\n At pH<\/p>\n Type A (Anaerobic) caused by tissue hypoxia<\/p>\n and<\/p>\n Type B (Aerobic)\u00a0 no evidence of hypoxia<\/p>\n <\/p>\n Type B is seen in DKA, certain cancers, and congenital diseases of the liver.<\/p>\n Lactates >9 are associated with a mortality of >75%<\/p>\n <\/p>\n Another review (Curr Opin Crit Care 2006;12:315)<\/p>\n <\/p>\n D-lactic acidosis<\/strong> is the stereoisomer seen in patients with short gut syndrome.<\/p>\n Uribarri J, Oh MS, Carroll HJ: D-lactic acidosis. A review of clinical presentation, biochemical features, and pathophysiologic mechanisms. Medicine (Baltimore) 1998; 72: 73-82<\/p>\n <\/p>\n D-Lactic acidosis Emergency physicians frequently are called upon to evaluate patients with an acute change in mental status. If the patient exhibits a metabolic acidosis, the clinician should consider D-Lactic acidosis as part of the differential diagnosis. Patients with this condition may complain of or appear to be drunk in the absence of ethanol intake. A unique form of lactic acidosis can occur in patients with jejunoileal bypass or, less commonly, small bowel resection or another cause of the short bowel syndrome. In these settings, glucose and starch are metabolized in the colon into D-lactic acid, which is then absorbed into the systemic circulation. Patients typically present with episodic metabolic acidosis (usually occurring after high carbohydrate meals) and characteristic neurologic abnormalities including confusion, cerebellar ataxia, slurred speech, and loss of memory. It is not clear if these symptoms are due to D-lactate itself or to some other toxin produced in the colon and then absorbed in parallel with D-lactate. The diagnosis of D-lactic acidosis should be strongly considered in the patient presenting with an increased serum anion gap, normal serum concentrations of lactate, and one or more of the following: Short bowel or other malabsorption syndrome Acidosis that is preceded by food intake and resolves with its discontinuation Characteristic neurologic symptoms and signs The standard assay for lactate will not detect D-lactate, hence serum concentrations of lactate will appear normal. Confirmation of the diagnosis requires a special enzymatic assay specifically testing for D-lactate. Therapy in this disorder consists of acute sodium bicarbonate administration to correct the acidemia and oral antimicrobial agents (such as metronidazole, neomycin, or vancomycin) to decrease the number of D-lactate producing organisms in the gut.<\/p>\n <\/p>\n D-Lactic Acidosis<\/strong>Emergency physicians frequently are called upon to evaluate patients with an acute change in mental status.\u00a0 If the patient exhibits a metabolic acidosis, the clinician should consider D-Lactic acidosis <\/em>as part of the differential diagnosis.\u00a0 Patients with this condition may complain of or appear to be drunk in the absence of ethanol intake.A unique form of lactic acidosis can occur in patients with jejunoileal bypass or, less commonly, small bowel resection or another cause of the short bowel syndrome. In these settings, glucose and starch are metabolized in the colon into D-lactic acid, which is then absorbed into the systemic circulation. Patients typically present with episodic metabolic acidosis (usually occurring after high carbohydrate meals) and characteristic neurologic abnormalities including confusion, cerebellar ataxia, slurred speech, and loss of memory. It is not clear if these symptoms are due to D-lactate itself or to some other toxin produced in the colon and then absorbed in parallel with D-lactate. The diagnosis of D-lactic acidosis should be strongly considered in the patient presenting with an increased serum anion gap, normal serum concentrations of lactate<\/em>, and one or more of the following:<\/p>\n The standard assay for lactate will not detect D-lactate, hence serum concentrations of lactate will appear normal. Confirmation of the diagnosis requires a special enzymatic assay specifically testing for D-lactate.Therapy in this disorder consists of acute sodium bicarbonate administration to correct the acidemia and oral antimicrobial agents (such as metronidazole, neomycin, or vancomycin) to decrease the number of D-lactate producing organisms in the gut. References: <\/em>(1) Stolberg, L, et al. D-Lactic acidosis due to abnormal gut flora\u00a0 N Engl J Med<\/em> 1982; 306:1344. (2) Halperin, ML, Kamel, KS. D-lactic acidosis: Turning sugars into acids in the gastrointestinal tract. Kidney Int<\/em> 1996; 49:1. (3) Uribarri, J, et al. D-lactic acidosis. Medicine<\/em> 1998; 77:73. (4) Mayne, AJ, et al. Dietary management of D-lactic acidosis in short bowel syndrome. Arch Dis Child <\/em>1990; 65:229. (5) Coronado, BE, Opal, SM, Yoburn, DC. Antibiotic-induced D-lactic acidosis.Ann Intern Med <\/em>1995; 122:839.<\/p>\n from emedhome<\/p>\n <\/p>\n <\/p>\n <\/p>\n In the River’s study, 1\/3 of folks with lactate>4 had bicarb >22 and anion gap\u00c3\u00a2\u00e2\u0080\u00b0\u00c2\u00a415<\/p>\n <\/p>\n <\/p>\n References: (1) Stolberg, L, et al. D-Lactic acidosis due to abnormal gut flora N Engl J Med 1982; 306:1344. (2) Halperin, ML, Kamel, KS. D-lactic acidosis: Turning sugars into acids in the gastrointestinal tract. Kidney Int 1996; 49:1. (3) Uribarri, J, et al. D-lactic acidosis. Medicine 1998; 77:73. (4) Mayne, AJ, et al. Dietary management of D-lactic acidosis in short bowel syndrome. Arch Dis Child 1990; 65:229. (5) Coronado, BE, Opal, SM, Yoburn, DC. Antibiotic-induced D-lactic acidosis. Ann Intern Med 1995; 122:839.<\/p>\n (Current Anaesthesia & Critical Care (2006) 17, 71\u00c3\u00a2\u00e2\u0082\u00ac\u00e2\u0080\u009c76)<\/p>\n pH = pKa+ log (H A\/HA)<\/p>\n 7:4 = 3.85 + log lactate \/lactic acid<\/p>\n <\/p>\n lactate to lactic acid 3548:1 at pH 7.4<\/p>\n Diagram from resus.me<\/p>\n Most severe form; pt will have enormous degree of lactic acidosis with hyperdynamic cardiac function. Should respond immediately to 100 mg thiamine. (Intensive Care Med (2005) 31:1004)<\/p>\n Thiamine deficiency<\/strong> should be considered in every case of severe lactic acidosis without an obvious cause, especially in high-risk populations (malnourished, alcoholics, Far-East workers, etc). (Journal of Emergency Medicine Volume 26, Issue 3 , April 2004, Pages 301-303)<\/p>\n <\/p>\n Alakalosis can cause lactate production because it stimulates glycolysis<\/p>\n Liver fx by itself can cause high blood lactate<\/p>\n Lactate ion<\/strong> itself in addition to the acidemia mat contribute to circulatory fx<\/p>\n If you give bicarb at all, give 1-2 mmol per kg by slow infusion<\/p>\n <\/p>\n Drugs known to be associated with type B2 lactic acidosis:<\/strong> acetaminophen, alcohols and glycols (ethanol, ethylene glycol, methanol, propylene glycol), almitrine, antiretroviral nucleoside analogs (zidovudine, delavirdine, didanosine, lamivudine, stavudine, zalcitabine), beta-adrenergic agents : epinephrine, ritodrine, terbutaline – but not salbutamol…, biguanides (phenformin, metformin), cocaine, cyanogenic compounds (eg, cyanide, aliphatic nitriles, nitroprusside), diethyl ether, 5-fluorouracil, halothane, iron, isoniazid, nalidixic acid, propofol, sugars and sugar alcohols (fructose, sorbitol, and xylitol), salicylates (eg, Reye syndrome), strychnine, sulfasalazine, and valproic acid. As you see, beta adrenergics can cause it, but salbutamol seems not to be reported yet. (Claudia)<\/p>\n <\/p>\n <\/p>\n =(Na (? + K)) \u00c3\u00a2\u00e2\u0082\u00ac\u00e2\u0080\u009c (Cl + Bicarb)<\/p>\n Correct for albumin by equation of Figge: AG + (0.25 x\u00a0(42 – albumin))\u00a0 \u00a0g\/L; if given in g\/dL, the factor is 2.5 (Crit Care Med 1998; 26:1807-1810)<\/p>\n Normal Gap 8-12 mEq\/L<\/p>\n Delta Gap=(AG-12)-(24-Bicarb) The increase in the AG should equate with the decrease in bicarb.<\/p>\n The concept is that there is a one to one relationship between the anion gap and decreased bicarb in pure anion gap acidosis.\u00a0 If there is not then there is either a combined non-anion gap acidosis or a metabolic acidosis depending on whether the delta gap is positive or negative.<\/p>\n <\/p>\n Anion Gap (AG)=2 x ALB + 0.5 (Phos)<\/p>\n <\/p>\n one article showed no increased discriminatory ability from correcting the anion gap for hypoalbuminemia (Emerg Med J 2006;23:627)<\/p>\n <\/p>\n With bicarbs>8 there should be a 1 mmHg drop in PaCO2 for every 1 meq\/dl fall in Bicarb.\u00a0 PCO2 can drop to ~12.<\/p>\n <\/p>\n Sodium Dichloroacetate (DCA):\u00a0 has the potential to decrease lactate levels and increase pH without the negative effects seen with bicarb.<\/p>\n Carbicarb:\u00a0 equimolar mixture sodium bicarb and sodium carbonate.\u00a0 Decrease CO2 instead of increasing it.<\/p>\n an exogenous buffer. Can lower PaCO2 and resolve acidosis. Lowers Sodium<\/p>\n Most Recent Study (J NEPHROL 2005; 18: 303-307<\/a>) sodium bicarbonate is contraindicated and THAM preferred in patients with mixed acidosis with high PaCO2 levels.<\/p>\n Review (acta anaes scand 2000;44:524)<\/p>\n Guidelines<\/a><\/p>\n Uremia-From H+ retention and from other organic acids<\/p>\n Salicylates-respiratory alkalosis, then met acidosis (uncoupling of oxidative phosporylation)<\/p>\n Methanol-wood alcohol.\u00a0 Becomes Formaldehyde and Formic Acid (blindness)<\/p>\n Ethylene Glycol-antifreeze.\u00a0 Urine will fluoresce.\u00a0 Kidney failure<\/p>\n Paraldehyde-Old medication<\/p>\n <\/p>\n <\/p>\n Cyanide, Carbon Monoxide<\/p>\n Alcoholic Ketoacidosis<\/p>\n Toluene, theophylline<\/p>\n <\/p>\n Methanol, Metformin, MetHb<\/p>\n Uremia (need BUN 50\/Cr 5)<\/p>\n Diabetic Ketoacidosis, Starvation Ketoacidosis<\/p>\n Paraldehyde,\u00a0 phenformin, Propylene Glycol<\/p>\n INH, Ibuprofen (high dose), IRON<\/p>\n Lactic Acidosis D (Blind GI Loops) and L (consider metformin, Type I), Lithium<\/p>\n Ethylene Glycol<\/p>\n Salicylates, strychnine<\/p>\n <\/p>\n If gap from lactate, should be 1:1, if not other acids are present.<\/p>\n <\/p>\n <\/p>\n High-dose lorazepam infusion is associated with high propylene glycol<\/strong> concentration, which may cause adverse effects. Therefore, PG accumulation and toxicity should be monitored for all patients receiving high-dose lorazepam for more than 48 hours. Potential adverse effects associated with high doses of PG include hyperosmolar metabolic acidosis, renal dysfunction, and intramuscular hemolysis in critically ill patients with normal renal function.<\/p>\n <\/p>\n Ativan and diazepam will cause propylene glycol toxicity causing anion gap and osmal gap acidosis. Anions are lactic acid. Versed does not need the propylene glycol because it is water soluble at low pH and fat soluble at body pH.<\/p>\n <\/p>\n A good portion of anion gap acidosis is probably caused by circulating members of the krebs cycle. These low molecular weight molecules were found in patients with lactic acidosis and DKA (Critical Care 2005;9:R591)<\/p>\n Sig in the critically ill<\/a><\/p>\n Chris from the Blunt Dissection has this approach:<\/p>\n The urinary anion gap can help to differentiate between GIT and renal causes of a hyperchloraemic metabolic acidosis.<\/p>\n NEGATIVE-UAG.<\/strong><\/p>\n POSITIVE-UAG.<\/strong><\/p>\n A group of disorders in which, due to either abnormal bicarbonate reabsorption <\/em>(proximal)\u00a0or\u00a0hydrogen ion excretion <\/em>(distal), results in development of a metabolic acidosis.<\/span><\/p>\n <\/p>\n Type 1.<\/strong><\/p>\n Type 2.<\/strong><\/p>\n Type 4.<\/strong><\/p>\n There are multiple case reports of Ibuprofen causing a distal RTA, usually when taken in\u00a0excessive doses.\u00a0 Such doses are most commonly taken in combination analgesics that also contain codeine.\u00a0 Although the mechanism is unknown it is postulated that it may involve inhibition of carbonic anhydrase.\u00a0 It may be associated with marked hypokalaemia and hypokalaemic paralysis.<\/p>\n <\/p>\n Any intestinal loss or RTAs<\/p>\n <\/p>\n physicochemical approach<\/a><\/p>\n I-Distal<\/strong><\/p>\n Impaired distal hydrogen ion secretion. Often accompanied by hypokalemia, low urinary NH4+, and hypocitraturia. Nephrolithiasis often occurs. Transient or persistent (classic adult form is associated with bicarb wasting and nerve deafness.) Mineral metabolism, hyperglobulinemic states, renal disease Myeloma.\u00a0 Urine pH<\/p>\n <\/p>\n II-Proximal<\/strong><\/p>\n impaired prox bicarb reabsorb. Vit d deficiency. Fanconi syndrome drugs like diamox, hyperparathyroidism, nephrotic syndrome\u00a0\u00a0 U pH>5.55 with bicarbonaturia. Bicarb is exhanged for Cl, which actually causes the acidosis<\/p>\n <\/p>\n IV-Hyperkalemic<\/strong><\/p>\n Intact acidification but impaired ammoniagenesis. Aldosterone deficienct. heparin, captopril, prostaglandin inhibitors. Increased K.\u00a0 Diabetics.<\/p>\n <\/p>\n <\/p>\n get UA and U lytes.\u00a0 Calculate urine anion gap.\u00a0 Urine (Na+K)-Cl.\u00a0 If negative then most likely a non-renal cause of non-anion gap acidosis.\u00a0 If positive, consider RTA.<\/p>\n <\/p>\n article on quant approach to RTA (crit care 2005;9)<\/p>\n <\/p>\n In pure met acidosis c compensation, last two digits of pH should=CO2<\/p>\n If pH<\/p>\n \u00a0<\/strong><\/p>\n Diarrhea<\/p>\n Ureterosigmoidostomy<\/p>\n Cholestyramine<\/p>\n Proximal renal tubular-acidosis<\/p>\n Renal insufficiency<\/p>\n Acetazolamide (Diamox)<\/p>\n <\/p>\n Inability to excrete H+<\/strong><\/p>\n Obstructive uropathy<\/p>\n Pyelonephritis<\/p>\n Hypoaldosteronism<\/p>\n Distal-renal tubular acidosis<\/p>\n Ingestion of ammonium chloride<\/p>\n Hyperalimentation<\/p>\n <\/p>\n The administration of sizable amounts of sodium bicarbonate\u00a0is associated with certain risks. Infusion of the\u00a0usual undiluted 1N <\/em>preparation (containing 1000 mmol of sodium\u00a0bicarbonate per liter) can give rise to hypernatremia and hyperosmolality.\u00a0This complication can be avoided by adding two 50-ml ampules\u00a0of sodium bicarbonate (each containing 50 mmol of sodium bicarbonate)\u00a0to 1 liter of 0.25 N<\/em> sodium chloride or three ampules to 1 liter\u00a0of 5 percent dextrose in water, thereby rendering these solutions\u00a0nearly isotonic. (NEJM 1998, 338(1), 26-34)<\/p>\n <\/p>\n <\/p>\n Forsythe SM, Schmidt GA. Sodium bicarbonate for the treatment of lactic acidosis. Chest 2000;117(1):260-7. Circumstances where it is appropriate to give bicarbonate:<\/p>\n Increased AG<\/strong><\/p>\n excessive exposure of sample to air causing carbonic acid decrease secondary to CO2 release<\/p>\n administration of poorly absorbed anionic abx (carbenicillin)<\/p>\n <\/p>\n Decreased AG<\/strong><\/p>\n halide, bromide, or iodide intox causing a false elevation of Cl<\/p>\n Hypertriglyceridemia causing false elev of Cl<\/p>\n Poorly absorbed cationic abx (polymyxin B)<\/p>\n hypoalbuminemia<\/p>\n <\/p>\n proof that stewart is much better than conventional s albumin correction (Crit Care Med 2007;35:1264)<\/p>\n Reunification of Acid-base physio (Critical Care 2005;9(5): )<\/a><\/p>\n Best Article on utility of Stewarts (Crit Care 2005;9(2):204)<\/a><\/p>\n Effects of Fluids<\/a><\/p>\n Acid Base in the ICU<\/a><\/p>\n <\/p>\n Obeserved BE + (sodium\/cl effect) – (albumin correction)=true base excess<\/p>\n <\/p>\n <\/p>\n When albumin is decreased, blood becomes more alkaline b\/c it is a weak acid<\/p>\n <\/p>\n <\/p>\n BE in whole blood, defined as the quantity (mM) of strong acid needed to restore pH to 7.4 in a blood sample equilibrated at PaCO2 = 40 mm Hg using the Van Slyke equation<\/p>\n <\/p>\n narrow Na Cl gap acidosis<\/p>\n It doesn’t change the H ion concentration. It causes more of the H ions to get dissociated. In other words the total H ions remain the same, but the free H ion activity increases. This changes the pH Lets imagine a container of pure water. Unlimited number of H ions, but almost no H is dissociated. Unlimited number of OH ions, but almost no OH is dissociated. Neutral pH . Neutral as in chemically neutral, not physiologically neutral. Add some strong ions to this pure water, say NaCl. Being strong ions, these will dissociate. The free Na will cause some OH to dissociate & the free Cl will cause an equal amount of H to dissociate. The amount of H & OH dissociated will be the same & hence the pH will still be “neutral”.<\/strong> Now take a fluid like blood with more Na (135) than Cl (100). More OH (135) is dissociated compared to H (100) & the pH will be alkalotic. Say the pH is 7.4. This is chemically alkalotic, but taken as the physiological neutral value. If this solution now had more Cl, with the same Na, relatively more H will be dissociated & the pH will fall, maybe to 7.3. The fall of the SID resulted in the pH becoming more acidic. This is because there were relatively more free or dissociated H ions are present in the solution after the SID decreased.<\/p>\n It does not use ATP. The equilibrium between lactate and pyruvate depends on the pH. If H+ concentration is high the equilibrium shifts to more lactate, if low, more pyruvate. Pyruvate is reduced to lactate by LDH (changes NADH to NAD) pH is -log[H+]<\/p>\n <\/p>\n Br J Anesthesia 2004;92(1):54-60<\/p>\n Am J Respir Crit Care Med 2000;162:2246.<\/p>\n <\/p>\n Lactic Acid (HLa) = Lactate- + H+ (99% disassociated at physiologic pH)<\/p>\n Heart and Brain can take up lactate and use for energy<\/p>\n RBCs shuttle lactate and take it to other areas of the body<\/p>\n Plasma carries 70% while RBCs carry 30%<\/p>\n <\/p>\n lactic acid metabolism (j applied physio\u00a0 558(1):29)<\/p>\n About erythrocyte metabolism. Erythrocytes use the Pentose Phosphate shunt (PPS) because it is the only way they can generate NADPH. Erythrocytes need NADPH to maintain a ready supply of reduced gluthathione, which is needed to combat oxidative stress. If the erythrocytes cannot use the PPS, they hemolyze. This is why people with G6PD deficiency (which is part of the PPS) hemolyze. Both Glycolysis and the PPS produce 3-P-glyceraldehide, which can be either converted to 2,3 DPG, or to Pyruvate and lactate. But the erythocyte contains as much 2,3 DPG as it does hemoglobin. So it produces relatively small quantities of lactate, as most of the 3-P-glyceraldehide is converted to 2,3 DPG.<\/p>\n <\/p>\n In patients with hepatic fx, lactate in solutions can increase serum lactate levels. Liver can process 100 mmol\/hour (Clin Endocrinol Metab 1980;9:513)<\/p>\n <\/p>\n Most commercial solutions have racemic lactate mixtures, the D-form is not measured by serum assay<\/p>\n <\/p>\n (Curr Opin Crit Care 1999;5(6):452)<\/p>\n is not a reliable indicator of anaerobic glycolysis<\/p>\n Dichloroacetate stims pyruvate dehydrogenase which converts pyruvate to acetyl CoA. This decreases lactate in septic patients without increasing oxygenation<\/p>\n another theory is regional anaerobiosis<\/p>\n more likely is that lactate metabolism is decreased in sepsis<\/p>\n Hyperventilation triples lactate in normal individuals: this is because cells do not take up lactate not b\/c of increased prod.<\/p>\n lungs may be source of excess lacate in sepsis<\/p>\n production may be aerobic representing cell stress from catecholamines<\/p>\n <\/p>\n (Anesth Analg 2003;96:919)<\/p>\n <\/p>\n Massive NaCl infusion causes met acidosis (J Trauma 2001;51(1):175)<\/p>\n <\/p>\n <\/p>\n (Curr Opin Crit Care 1999;5(6):436)<\/p>\n water is a weak acid (pKa 13.5 at 40 C) as temp goes up, it gets more acidic<\/p>\n free water therefore causes acidosis when given to correct hyponatremia<\/p>\n This is because free water causes Na to fall in greater degree than Cl<\/p>\n <\/p>\n Dextrose makes solutions even more acidic, b\/c it forms acid after oxidation. That is until it is metabolized<\/p>\n <\/p>\n Multicarbon ions such as acetate and gluconate are usually taken up by cells within minutes. The actual metabolism of these ions may further decrease acidosis.<\/p>\n <\/p>\n If packaging is in bags instead of glass, CO2 will diffuse in, which alters bicarb concentrations; this is why multicarbons are used<\/p>\n <\/p>\n <\/p>\n (Curr Opin Crit Care 1999;5(6):440)<\/p>\n colloid is a state of matter that is neither solution or suspension; defined by ability to move molecules across membranes<\/p>\n Albumin 20% has a mild acidifying effect (Intensive Care Med (2005) 31:1123\u00c3\u00a2\u00e2\u0082\u00ac\u00e2\u0080\u009c1127)<\/p>\n <\/p>\n <\/p>\n (Curr Opin Crit Care 1999;5(6):443)<\/p>\n In patients with liver failure, multicarbon anions will not be metabolized and CVVH will cause acidosis. In these folks, bicarb solutions must be used<\/p>\n Lactate is not cleared by hemofilter, so serum levels are still accurate if substitution fluid is not lactate containing<\/p>\n <\/p>\n Bicarb solutions can be kept shelf-safe by using two bags, one with 4.75 L of bicarb-free solutions and a 250 cc glass bottle of bicarb solution containing 160 mmol NaBicarb (Hemosol) Double spike delivers bicarb to bag just before use.<\/p>\n <\/p>\n Acid Base of HD (Curr Opin Crit Care 1999;5(6):468)<\/p>\n four defense mechanisms to our daily acid load:<\/p>\n ion transport across cell membranes<\/p>\n removal of co2 by lungs<\/p>\n kidney ion elimination<\/strong><\/p>\n liver metabolism<\/p>\n <\/p>\n renal failure causes hyperchloremic acidosis and then high anion gap acidosis<\/p>\n this causes decreased cardiac contractility<\/p>\n and altered response to drugs<\/p>\n <\/p>\n SID of HD dialysate is usually 40<\/p>\n <\/p>\n Lactate and the Kidney (Critical Care 2002;6(4))<\/p>\n kidney second only to the liver in the ability to remove lactate from the circulation and metabolizing it<\/p>\n very little is actually excreted in the urine confined to cortex; medulla actually creating lactate from glycolysis<\/p>\n <\/p>\n <\/p>\n Diamox works by excretion of sodium without chloride (Critical Care 2006;10:R14)<\/p>\n <\/p>\n SBE = 0.9287 \u00c3\u0083\u00e2\u0080\u0094 (HCO3- – 24.4 + 14.83 \u00c3\u0083\u00e2\u0080\u0094 [pH – 7.4])<\/p>\n <\/p>\n Corrected Base Excess=BE-(Na-Cl-38)-(2.5(4.2-Albumin in g\/dl))<\/strong><\/p>\n <\/p>\n Each 1 g\/dl albumin has a charge of 2.8 mEq\/l at pH 7.4 (2.3 mEq\/l at 7.0 and 3.0 mEq\/l at 7.6), and each 1 mg\/dl phosphate has a charge of 0.59 mEq\/l at pH 7.4 (0.55 mEq\/l at 7.0 and 0.61 mEq\/l at 7.6). Thus, in much the same way that the corrected SBE equation (Eqn 5) updates BE to allow for changes in ATOT, the AG may be corrected to yield a corrected AG (AGc)<\/p>\n <\/p>\n SIG = ([Na+ + K+ + Ca2+ + Mg2+] – [Cl- + lactate-]) – (2.46 \u00c3\u0083\u00e2\u0080\u0094 10-8 \u00c3\u0083\u00e2\u0080\u0094 PCO2\/10-pH + [albumin (g\/dl)] \u00c3\u0083\u00e2\u0080\u0094 [0.123 \u00c3\u0083\u00e2\u0080\u0094 pH – 0.631] + [PO4- (mmol\/l) \u00c3\u0083\u00e2\u0080\u0094 (pH – 0.469)])<\/p>\n <\/p>\n SIDm=Na + K + 2(Mg) +2(Ca) – Cl – lactate – urate<\/p>\n <\/p>\n Importantly, all the strong ions are expressed in mEq\/l and only the ionized portions of Mg2+ and Ca2+ are considered (to convert total to ionized Mg2+, multiply by 0.7). Note also that we do not consider lactate as unmeasured. Because the concentration of unmeasured anions is expected to be quite low (<\/p>\n <\/p>\n Br J Anaesth 2004;92(1):54-60)<\/p>\n Sodium Cl effect (meq\/l)=Na – Cl – 38<\/p>\n Albumin Effect (meq\/l)=(0.123 x pH – 0.631) x (42-albumin (g\/l))<\/p>\n =0.25 x (42-albumin (g\/l)<\/p>\n =2.5 x (4.2 – albumin (g\/dl)<\/p>\n Corrected Base Excess (meq\/l)=BEm – (Na – Cl – 38) – (2.5 x (4.2-albumin)<\/p>\n Am J Respir Crit Care Med 2000;162:2246<\/p>\n Pi-=(Pi) x (0.309 x pH -0.469)<\/p>\n XA-=other strong ions: lactate, ketoacids, sulfate<\/p>\n 1.8 (Pi mmol\/L)<\/p>\n Mixing Dialysis fluids can use NaAcetate or NaBicarb to balance NaCl<\/p>\n In massive fluid resus such as cardiopulmonary bypass priming, then move closer to 24 for SID to make up for dilution of albumin<\/p>\n Hyproteinemia, SID, and acid base in the crit ill (J appl physio 1998;1740)<\/p>\n serum acid-base may be misaltered b\/c of compensation for csf acid-base<\/p>\n so hypoproteinemia may actually result in hyperventilation<\/p>\n <\/p>\n Fundamental Principles of Acid-Base (Critical Care 2005;9(2):)<\/p>\n <\/p>\n <\/p>\n SIG=AG – [albumin (g\/dl)] (1.2 \u00c3\u0083\u00e2\u0080\u0094 pH-6.15) – [phosphate (mg\/dl)] (0.097 \u00c3\u0083\u00e2\u0080\u0094 pH-0.13)<\/p>\n <\/p>\n see above<\/p>\n <\/p>\n Disease states classified according to the Stewart approach<\/strong>\u00a0 Acid\u00c3\u00a2\u00e2\u0082\u00ac\u00e2\u0080\u009cbase disturbance \u00a0 Disease state \u00a0 Examples \u00a0 Metabolic alkalosis \u00a0 Low serum albumin \u00a0 Nephrotic syndrome, hepatic cirrhosis \u00a0 \u00a0 High SID+ \u00a0 Chloride loss: vomiting, gastric drainage, diuretics, post-hypercapnea, Cl- wasting diarrhea due to villous adenoma, mineralocorticoid excess, Cushing’s syndrome, Liddle’s syndrome, Bartter’s syndrome, exogenous corticosteroids, licorice Na2+ load (such as acetate, citrate, lactate): Ringer’s solution, TPN, blood transfusion \u00a0Metabolic acidosis \u00a0 Low SID+ and high SIG \u00a0 Ketoacids, lactic acid, salicylate, formate, methanol \u00a0 \u00a0 Low SID+ and low SIG \u00a0 RTA, TPN, saline, anion exchange resins<\/p>\n <\/p>\n gelatin from some colloids is a weak acid<\/p>\n free water is an acid, b\/c it has a SID of 0<\/p>\n <\/p>\n SBE=0.93 x ((Bicarb) + 14.84 x (pH – 7.4) – 24.4)<\/p>\n <\/p>\n Equivalent strong ion difference reductions by adding 1 l water or 1 l of 0.15 mol\/l NaCl to a 3 l sample of mock extracellular fluid<\/strong>\u00a0 \u00a0 ‘ECF’ \u00a0 After saline dilution \u00a0 After water dilution \u00a0 [Na+] \u00a0 140 \u00a0 142.5 \u00a0 105 \u00a0[Cl-] \u00a0 100 \u00a0 112.5 \u00a0 75 \u00a0[A-] + [HCO3 -] \u00a0 40 \u00a0 30 \u00a0 30 \u00a0SID \u00a0 40 \u00a0 30 \u00a0 30<\/p>\n <\/p>\n <\/p>\n If met alkalosis is assoc c decreased serum K, then KCl is a great way to correct as it has a SID of 0 which actually becomes neg as k is taken up<\/p>\n <\/p>\n ‘Balanced’ crystalloids To avoid crystalloid induced acid\u00c3\u00a2\u00e2\u0082\u00ac\u00e2\u0080\u009cbase disturbances, plasma SID must fall just enough during rapid infusion to counteract the progressive ATOTdilutional alkalosis. Balanced crystalloids thus must have a SID lower than plasma SID but higher than zero. Experimentally, this value is 24 mEq\/l [23,43]. In other words, saline can be ‘balanced’ by replacing 24 mEq\/l of Cl- with OH-, HCO3 – or CO3 2-. From this perspective, and for now ignoring pH, solutions 1 and 3 in Table 4 are ‘balanced’. However, it is noteworthy that, unless stored in glass, solutions 1 and 3 both become solution 2 by gradual equilibration with atmospheric CO2 (Table 4). Solution 2 is also ‘balanced’. To eliminate the issue of atmospheric equilibration, commercial suppliers have substituted various organic anions such as L-lactate, acetate, gluconate and citrate as weak ion surrogates. Solution 4 (Table 4) is a generic example of this approach (for actual examples, see Table 5). L-lactate is a strong anion, and the in vitro SID of solution 4 is zero. However, solution 4 can also be regarded as ‘balanced’, provided L-lactate is metabolized rapidly after infusion. In fact, in the absence of severe liver dysfunction, L-lactate can be metabolized at rates of 100 mmol\/hour or more [44,45], which is equivalent to nearly 4 l\/hour of solution 4. The in vivo or ‘effective’ SID of solution 4 can be calculated from the L-lactate component subject to metabolic ‘disappearance’. If the plasma [lactate] stays at 2 mmol\/l during infusion, then solution 4 has an effective SID of 24 mEq\/l. Hence, despite wide variation in pH, solutions 1\u00c3\u00a2\u00e2\u0082\u00ac\u00e2\u0080\u009c4 in Table 4 have identical effective SID values. They are all ‘balanced’, with identical systemic acid\u00c3\u00a2\u00e2\u0082\u00ac\u00e2\u0080\u009cbase effects. However, other attributes must be considered. Solution 1 (pH 12.38) is too alkaline for peripheral or rapid central administration. The situation for solution 2 is less clear. Atmospheric equilibration has brought the pH to 9.35, which is less than that of sodium thiopentone (pH 10.4) [46] \u00c3\u00a2\u00e2\u0082\u00ac\u00e2\u0080\u009c a drug that is normally free of venous irritation. Similarly Carbicarb, a low CO2TOT alternative to NaHCO3 preparations [47], has a pH of 9.6 [48]. Thus, the pH of solution 2 may not preclude peripheral or more rapid central administration. On the downside, and like Carbicarb, solution 2 contains significant concentrations of carbonate, which precipitates if traces of Ca2+ or Mg2+ are present. A chelating agent such as sodium edetate may be required.<\/p>\n <\/p>\n Four balanced crystalloids (see text)<\/strong>\u00a0 \u00a0 Solution 1 \u00a0 Solution 2 \u00a0 Solution 3 \u00a0 Solution 4 \u00a0 [Na+] \u00a0 140 \u00a0 140 \u00a0 140 \u00a0 140 \u00a0[Cl-] \u00a0 116 \u00a0 116 \u00a0 116 \u00a0 114 \u00a0[HCO3 -] \u00a0 \u00a0 19.2 \u00a0 24 \u00a0 \u00a0[CO3 2-] \u00a0 \u00a0 4.8 \u00a0 \u00a0 \u00a0[OH-] \u00a0 24 \u00a0 \u00a0 \u00a0 \u00a0[L-lactate] \u00a0 \u00a0 \u00a0 \u00a0 26 \u00a0PCO2 (mmHg) \u00a0 0 \u00a0 0.3a \u00a0 760 \u00a0 0.3a \u00a0pH \u00a0 12.38 \u00a0 9.35 \u00a0 6.04 \u00a0 6.49 \u00a0Effective SID \u00a0 24 \u00a0 24 \u00a0 24 \u00a0 24<\/p>\n <\/p>\n <\/p>\n <\/p>\n Six colloid solutions<\/strong>\u00a0 \u00a0 Albumex 4 \u00a0 Haemaccel \u00a0 Gelofusine \u00a0 PENTASPAN \u00a0 HESpan \u00a0 Hextend \u00a0 [Albumin]b \u00a0 40 g\/l \u00a0 \u00a0 \u00a0 \u00a0 \u00a0 \u00a0[Gelatin urea-linked]b \u00a0 \u00a0 35 g\/l \u00a0 \u00a0 \u00a0 \u00a0 \u00a0[Gelatin succinylated]b \u00a0 \u00a0 \u00a0 40 g\/l \u00a0 \u00a0 \u00a0 \u00a0[Pentastarch] \u00a0 \u00a0 \u00a0 \u00a0 100 g\/l \u00a0 \u00a0 \u00a0[Hetastarch] \u00a0 \u00a0 \u00a0 \u00a0 \u00a0 60 g\/l \u00a0 60 g\/l \u00a0[Na+] \u00a0 140 \u00a0 145 \u00a0 154 \u00a0 154 \u00a0 154 \u00a0 143 \u00a0[K+] \u00a0 \u00a0 5.1 \u00a0 \u00a0 \u00a0 \u00a0 3 \u00a0[Ca2+] \u00a0 \u00a0 12.5 \u00a0 \u00a0 \u00a0 \u00a0 5 \u00a0[Mg2+] \u00a0 \u00a0 \u00a0 \u00a0 \u00a0 \u00a0 0.8 \u00a0[Cl-] \u00a0 128 \u00a0 145 \u00a0 120 \u00a0 154 \u00a0 154 \u00a0 124 \u00a0[L-lactate] \u00a0 \u00a0 \u00a0 \u00a0 \u00a0 \u00a0 28 \u00a0[Glucose] \u00a0 \u00a0 \u00a0 \u00a0 \u00a0 \u00a0 5.5 \u00a0[Octanoate] \u00a0 6.4 \u00a0 \u00a0 \u00a0 \u00a0 \u00a0 \u00a0Effective SID \u00a0 12 \u00a0 17.6 \u00a0 34 \u00a0 0 \u00a0 0 \u00a0 26a \u00a0 aAssumes stable plasma lactate concentrations of 2 mmol\/L (see text). bWeak acid. Electrolyte concentrations are given in mEq\/l. SID, strong ion difference.<\/p>\n <\/p>\n <\/p>\n Blood At collection, blood is mixed with a preservative, normally CPDA-1 [68], providing approximately 17 mEq trivalent citrate anions per unit, and a small amount of phosphate [69]. The accompanying sodium cation adds about 40 mEq\/l to the effective SID of whole blood. For this reason it is not surprising that large volume whole blood transfusion commonly results in a post-transfusion metabolic alkalosis (following citrate metabolism). With packed red cells, the standard red cell preparation in most countries, the preservative load per blood unit is reduced. Nevertheless, large volume replacement with packed red cells still produces metabolic alkalosis [69]. Conversely, if liver dysfunction is severe enough to block or grossly retard citrate metabolism, then the problem becomes ionized hypocalcaemia and metabolic acidosis [70]. sulphates are the strong anions in renal failure<\/p>\n <\/p>\n ng suction without proton pump inhibition cause alkalosis from cl loss<\/p>\n <\/p>\n lactic acidemia vs. hyperlactatemia<\/p>\n <\/p>\n acidosis screws up coagulation<\/p>\n van slyke is accurate in vivo (crit care med 2000;28(8):2932)<\/p>\n <\/p>\n Acid Base of RRT<\/p>\n phosphate x (0.309 x (pH-0.469))<\/p>\n <\/p>\n 1000 x 2.46 x 10-11 x PCO2\/( 10-pH )<\/p>\n <\/p>\n possible unmeasured anions in uremia are sulfate, urate, hydroxypropionate, oxalate, furanpropionate<\/p>\n <\/p>\n if pt’s liver can not metabolize citrate, it will stay in the blood stream and chelate calcium and act as a strong anion causing met acidosis<\/p>\n <\/p>\n CVVH may have a sieving constant of >1 causing met alkalosis even with well designed fluids<\/p>\n <\/p>\n<\/span>Interpreting ABGs<\/span><\/h2>\n
<\/span>Acidemia<\/span><\/h2>\n
<\/span>Metabolic Acidosis<\/span><\/h3>\n
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Hypercapnic Metabolic Acidosis<\/h4>\n
DKA<\/h4>\n
NaBicarb Administration<\/h4>\n
<\/span>Lactic Acidosis<\/span><\/h3>\n
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Lactate Metabolism<\/h4>\n
![\"\"](\"\/wp-content\/images\/part1\/lactatemetab_small.jpg\")
<\/a><\/p>\n![\"lactate](\"\/wp-content\/images\/part5\/lactates%20from%20resus.me_small.jpg\")
<\/a><\/p>\nShoshin Beri Beri<\/h4>\n
<\/span>Cori Cycle<\/span><\/h3>\n
![\"\"](\"\/wp-content\/images\/part1\/615coricycle_small.gif\")
<\/a>![\"\"](\"\/wp-content\/images\/part1\/cori%20cycle2_small.jpg\")
<\/a>![\"\"](\"\/wp-content\/images\/part1\/kreb%20cycle2_small.jpg\")
<\/a><\/p>\n<\/span>Aspirin<\/a><\/span><\/h3>\n
<\/span>Anion Gap<\/span><\/h2>\n
<\/span>THAM<\/span><\/h2>\n
<\/span>High Anion Gap (CAT MUDPILES)<\/span><\/h3>\n
<\/h3>\n
<\/span>Unknown Cause of High Sig in the Critically Ill<\/span><\/h2>\n
<\/span>Normal Anion Gap<\/span><\/h2>\n
![\"USEDCARP\"](\"https:\/\/crashingpatient.com\/wp-content\/uploads\/2011\/09\/USEDCARP.png\")
<\/a><\/p>\n<\/span>
![\"\"](\"https:\/\/crashingpatient.com\/wp-content\/uploads\/2011\/09\/Figure-2-Gamblegram-Urinary-Anion-Gap-RTA-Joel-Topf.png\")
<\/a>URINARY ANION GAP [UAG].<\/strong><\/span><\/h3>\n\n
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<\/span>Renal tubular acidosis.<\/span><\/h2>\n
<\/span>The basics.<\/strong><\/span><\/h3>\n
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![\"RTA-table\"](\"https:\/\/crashingpatient.com\/wp-content\/uploads\/2011\/09\/RTA-table-600x161.png\")
<\/a><\/p>\n<\/span>Causes.<\/span><\/h3>\n
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<\/span>Specific to this case\u2026<\/strong><\/span><\/h3>\n
<\/span>Management.<\/strong><\/span><\/h3>\n
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Renal Tubular Acidosis<\/h4>\n
Loss of HCO3 –<\/h4>\n
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<\/span>Low Anion Gap<\/span><\/h2>\n
![\"\"](\"\/wp-content\/images\/part1\/13FFB3.gif\")
![\"\"](\"\/wp-content\/images\/part1\/13FFB4.gif\")
<\/p>\nSources of Error: Pseudo-Met Acidosis<\/h4>\n
<\/span>Strong Ion Approach<\/span><\/h2>\n
![\"\"](\"\/wp-content\/images\/part1\/gamblegram_small.jpg\")
<\/a><\/p>\nArticles<\/h4>\n
\n
![\"\"](\"\/wp-content\/images\/part1\/0001@483_S03351-062-u015.jpg\")
![\"\"](\"\/wp-content\/images\/part1\/0002@483_S03351-062-u016.jpg\")
![\"\"](\"\/wp-content\/images\/part1\/0003@483_S03351-062-u017.jpg\")
![\"\"](\"\/wp-content\/images\/part1\/0004@483_S03351-062-u018.jpg\")
<\/p>\nLactate in Sepsis<\/h4>\n
Hyperchloremic Acidosis<\/h4>\n
Acid Base Physiology of Crystalloids<\/h4>\n
Acid Base of Colloids<\/h4>\n
Acid Base and Renal Failure, CVVH\u00a0 and Hemodialysis<\/h4>\n
<\/span>Formulas<\/span><\/h3>\n
![\"\"](\"\/wp-content\/images\/part1\/gamblegram_small.gif\")
<\/a>![\"\"](\"\/wp-content\/images\/part1\/integratedstewart_small.gif\")
<\/a><\/p>\n<\/span>Method IV Fencl-Stewart<\/span><\/h2>\n
<\/span>Acidosis of Cardiac Arrest<\/span><\/h3>\n