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Metabolic Acidosis Litfl

Metabolic Acidosis Archives Life In The Fast Lane Litfl Medical Blog

Metabolic Acidosis Archives Life In The Fast Lane Litfl Medical Blog

Questions26.1The following results are from the arterial blood gas analysis of a 46-year-old male ventilatedin ICU for three weeks with severe community-acquired pneumonia and ARDS:a) Describe the abnormalities.b) Give one likely cause.26.2A 75-year-old female insulin-dependent diabetic presents to the Emergency Department semi-comatose. She has been [Read more...] about CICM SAQ 2013.2 Q26 Questions18.1 A 62-year-old female is brought into hospital with suspected organophosphate poisoning.a) List six acute clinical features associated with this condition.b) List the antidotes indicated in this condition and the rationale for their use.The following data are taken from this patient:c) What does the result of the mixing test [Read more...] about CICM SAQ 2013.2 Q18 QuestionsA 56 year old, homeless man was admitted to the Emergency Department with clinical features suggestive of a bowel obstruction. As he is confused, it is not possible to elicit a clear history.The first set of blood tests show: a) Outline the possible causes of his metabolic acidosis.b) What is the corrected serum sodium?c) Outline your approach to [Read more...] about CICM SAQ 2010.2 Q19 Question15. The following blood gases obtained at 8am and 10 am from a patient admitted to the ICU with Grade V Subarachnoid hemorrhage. Between the two sets of arterial blood gases a procedure was performed. Changes in gas tensions were not accompanied by changes in haemodynamic parameters.15.1 What procedure was performed? Give reasons.15.2 A 41 year old [Read more...] about CICM SAQ 2009.2 Q15 aka Metabolic Muddle 009A 26 year old male presents with nausea, vomiting and confusion. The following blood gas is obtained on admissionpH 7.24 (7.35-7.45)pCO2 27 (35-45)paO2 91 [Read more...] about Young and Yellow Continue reading >>

High Anion Gap Metabolic Acidosis

High Anion Gap Metabolic Acidosis

When acidosis is present on blood tests, the first step in determining the cause is determining the anion gap. If the anion gap is high (>12 mEq/L), there are several potential causes. High anion gap metabolic acidosis is a form of metabolic acidosis characterized by a high anion gap (a medical value based on the concentrations of ions in a patient's serum). An anion gap is usually considered to be high if it is over 12 mEq/L. High anion gap metabolic acidosis is caused generally by acid produced by the body,. More rarely, high anion gap metabolic acidosis may be caused by ingesting methanol or overdosing on aspirin.[1][2] The Delta Ratio is a formula that can be used to assess elevated anion gap metabolic acidosis and to evaluate whether mixed acid base disorder (metabolic acidosis) is present. The list of agents that cause high anion gap metabolic acidosis is similar to but broader than the list of agents that cause a serum osmolal gap. Causes[edit] Causes include: The newest mnemonic was proposed in The Lancet reflecting current causes of anion gap metabolic acidosis:[3] G — glycols (ethylene glycol & propylene glycol) O — oxoproline, a metabolite of paracetamol L — L-lactate, the chemical responsible for lactic acidosis D — D-lactate M — methanol A — aspirin R — renal failure K — ketoacidosis, ketones generated from starvation, alcohol, and diabetic ketoacidosis The mnemonic MUDPILES is commonly used to remember the causes of increased anion gap metabolic acidosis.[4][5] M — Methanol U — Uremia (chronic kidney failure) D — Diabetic ketoacidosis P — Paracetamol, Propylene glycol (used as an inactive stabilizer in many medications; historically, the "P" also stood for Paraldehyde, though this substance is not commonly used today) I — Infectio Continue reading >>

Acid Base Disorders

Acid Base Disorders

Arterial blood gas analysis is used to determine the adequacy of oxygenation and ventilation, assess respiratory function and determine the acid–base balance. These data provide information regarding potential primary and compensatory processes that affect the body’s acid–base buffering system. Interpret the ABGs in a stepwise manner: Determine the adequacy of oxygenation (PaO2) Normal range: 80–100 mmHg (10.6–13.3 kPa) Determine pH status Normal pH range: 7.35–7.45 (H+ 35–45 nmol/L) pH <7.35: Acidosis is an abnormal process that increases the serum hydrogen ion concentration, lowers the pH and results in acidaemia. pH >7.45: Alkalosis is an abnormal process that decreases the hydrogen ion concentration and results in alkalaemia. Determine the respiratory component (PaCO2) Primary respiratory acidosis (hypoventilation) if pH <7.35 and HCO3– normal. Normal range: PaCO2 35–45 mmHg (4.7–6.0 kPa) PaCO2 >45 mmHg (> 6.0 kPa): Respiratory compensation for metabolic alkalosis if pH >7.45 and HCO3– (increased). PaCO2 <35 mmHg (4.7 kPa): Primary respiratory alkalosis (hyperventilation) if pH >7.45 and HCO3– normal. Respiratory compensation for metabolic acidosis if pH <7.35 and HCO3– (decreased). Determine the metabolic component (HCO3–) Normal HCO3– range 22–26 mmol/L HCO3 <22 mmol/L: Primary metabolic acidosis if pH <7.35. Renal compensation for respiratory alkalosis if pH >7.45. HCO3 >26 mmol/L: Primary metabolic alkalosis if pH >7.45. Renal compensation for respiratory acidosis if pH <7.35. Additional definitions Osmolar Gap Use: Screening test for detecting abnormal low MW solutes (e.g. ethanol, methanol & ethylene glycol [Reference]) An elevated osmolar gap (>10) provides indirect evidence for the presence of an abnormal solute which is prese Continue reading >>

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 >>

Acid Base Disorders And Osmolar Gaps

Acid Base Disorders And Osmolar Gaps

This is quick reference page to acid base disorders in toxicology and osmolar gaps. Zeff a toxicologist from Melbourne talks through his approach and the errors that can occur with osmolar and anion gaps. Step 2: Determine whether the primary process is reparatory, metabolic or both. A respiratory disturbance alters PaCO2 and metabolic disturbance alters the serum HCO3: Step 3: Acute or chronic respiratory disturbance? In acute disturbances the pH changes 0.08 for every 10 mmHg PaCO2 varies from 40. 1-2-HCO3-4-5 rule for change in HCO3 for every 10 mmPaCO2 varies from 40: Acute respiratory acidosis HCO3 increases by 1 Acute respiratory alkalosis HCO3 decreases by 2 Chronic respiratory acidosis HCO3 increases by 4 Chronic respiratory alkalosis HCO3 decreases by 5 Step 4: Determine if anion gap present for metabolic acidosis. Step 5: Expected respiratory compensation. In Metabolic acidosis the change in PaCO2 is in linear correlation with the change in HCO3 (the drop in HCO3 should be matched by the same change in increased PaCO2). If expected PaCO2 falls outside range, then theres an additional respiratory disturbance. In metabolic alkalosisthe response is hypoventilation, therefore the change is not linear. It will not increase greater than 50-55 to compensate for a metabolic alkalosis. Also a patient will be alkalaemic if PaCO2 is elevated to compensate for a metabolic alkalosis. If academic, then an additional respiratory acidosis is present. Expected pCO2 = 0.7[HCO3] + 20 (range +/- 5) Step 6: Determine whether other metabolic disturbances co-exist with anion gap acidosis. A non-anion gap acidosis or a metabolic alkalosis may co-exist. Corrected HCO3 = measured HCO3 + (anion gap 12) If corrected HCO3 >24, metabolic alkalosis co-exists If corrected HCO3 <24, non-anio Continue reading >>

Anion Gap

Anion Gap

OVERVIEW Anion Gap = Na+ – (Cl- + HCO3-) The Anion Gap (AG) is a derived variable primarily used for the evaluation of metabolic acidosis to determine the presence of unmeasured anions The normal anion gap depends on serum phosphate and serum albumin concentrations An elevated anion gap strongly suggests the presence of a metabolic acidosis The normal anion gap varies with different assays, but is typically 4 to 12mmol/L (if measured by ion selective electrode; 8 to 16 if measured by older technique of flame photometry) If AG > 30 mmol/L then metabolic acidosis invariably present If AG 20-29mmol/L then 1/3 will not have a metabolic acidosis K can be added to Na+, but in practice offers little advantage ALBUMIN AND PHOSPHATE the normal anion gap depends on serum phosphate and serum albumin the normal AG = 0.2 x [albumin] (g/L) + 1.5 x [phosphate] (mmol/L) albumin is the major unmeasured anion and contributes almost the whole of the value of the anion gap. every 1g/L decrease in albumin will decrease anion gap by 0.25 mmoles a normally high anion gap acidosis in a patient with hypoalbuminaemia may appear as a normal anion gap acidosis. this is particularly relevant in ICU patients where lower albumin levels are common HIGH ANION GAP METABOLIC ACIDOSIS (HAGMA) HAGMA results from accumulation of organic acids or impaired H+ excretion Causes (LTKR) Lactate Toxins Ketones Renal Causes (CATMUDPILES) CO, CN Alcoholic ketoacidosis and starvation ketoacidosis Toluene Metformin, Methanol Uremia DKA Pyroglutamic acidosis, paracetamol, phenformin, propylene glycol, paraladehyde Iron, Isoniazid Lactic acidosis Ethylene glycol Salicylates Effects of albumin Anion gap may be underesitmated in hypoalbuminaemia, because if albumin decreased by 1g/L then the anion gap decreases by 0.25 Continue reading >>

Metabolic Muddle Litfl Clinical Cases Catmudpiles

Metabolic Muddle Litfl Clinical Cases Catmudpiles

The first step: is the patient acidaemic or alkalaemic? The second step: is there a metabolic acidosis or a respiratory acidosis or both? The third step: is there appropriate compensation? The estimated expected CO2 is 1.5xHCO3 + 8 i.e. approximately 13 so its pretty close The fourth step: what is the nature of the metabolic acidosis? The anion gap is markedly elevated at 35 [(Na+ K+) (Cl-+HCO3-)] The fifth step: is there a coexistent normal anion gap acidosis or pre-existing metabolic alkalosis? If the high anion gap acidosis is the only metabolic disturbance, the bicarbonate drops by the same degree that the anion gap rises. In this case, assuming a normal anion gap of 12, the anion gap has increased by 23 while the HCO3- has decreased by 23.Assuming a normal HCO3- of 26 the bicarbonate has decreased by 23 to finish up at 3. So the high anion gap metabolic acidosis is the only metabolic disturbance. If the bicarbonate drops less than anticipated, it must have started off at a higher level than you normally expect (i.e. there must be a pre-existing metabolic alkalosis) If the bicarbonate drops more than anticipated, there must be another source of acidosis (i.e. a co-existent normal anion gap acidosis) Continue reading >>

Metabolic Muddle Litfl Clinical Cases Staph Sepsis Acidosis

Metabolic Muddle Litfl Clinical Cases Staph Sepsis Acidosis

Given that the lactate and ketones are normal the most likely cause is: pyroglutamic acidemia (aka 5-oxoprolinemia) This can be confirmed by performing a metabolic screen for urinary organic acids. Blood levels may be required if the patient is anuric. An elevated level of pyroglutamic acid confirms the diagnosis. Skip this one if youre biochemically challenged 5-oxoproline (aka pyroglutamic acid) is produced from -glutamyl cysteine by the enzyme -glutamyl cyclotransferase. This enzymes activity increases when glutathione levels are low, due to a loss of feedback inhibition from glutathione. Thus the accumulation of pyroglutamic acid is thought to be due to depletion of the glutathione, particularly when glutathione synthetase is inhibited. Decreased activity of 5-oxoprolinase, which breaks down pyroglutamic acid, may also play a role. Check out the -glutamyl cycle to see how this all links up: Key: A = excess -glutamyl cysteine becomes a substrate for -glutamyl cyclotransferase, P = paracetamol, S = sepsis, F = flucloxacillin. From Dempsey et al, 2000. See also Q5. Continue reading >>

Hypokalaemia And Metabolic Acidosis

Hypokalaemia And Metabolic Acidosis

Home | Education | Hypokalaemia and Metabolic Acidosis 35 year old Aboriginal female presents with a 2/52 Hx of weakness, thirst and nausea. Presents to ED unable to lift her hands. Admitted 3/12 ago with something similar but doesnt know what it was and her medical notes are not immediately available. No other past medical history of note. Examination reveals a quiet, dehydrated lady with generalised non-lateralising weakness in all 4 limbs. Bedside venous blood gas results included: Sinus rhythm with sinus arrhythmia at a rate of 72 bpm. U waves noted most prominently in leads V1-V3 Sinus arrhythmia [sinus rhythm with slight variation (>0.16 seconds) in the sinus cycles] Normal anion gap metabolic acidosis. The 2 most common causes in ED Other causes are many and varied. There are several mnemonics out there the most recent edition of Rosen suggests: F-USED CARS Basically (and rather obviously), a metabolic acidosis is caused by either excess acid or a loss of alkali. Excess acid may be produced by the body itself or may be exogenous. Calculating the anion gap is used in the context of having made a diagnosis of a metabolic acidosis to help determine possible causes. Its an artificial but pragmatic concept based on the fact that with normal physiology there will be more unmeasured anions (predominantly Albumin, Phosphate and Sulphate) than cations on routine blood testing. Most people dont use potassium in the equation resulting in a normal range of 8-12. (12-16 if potassium included), although in this case it wouldnt have made much difference! A wide anion gap in the setting of a metabolic acidosis (or High Anion Gap Metabolic Acidosis [HAGMA]) suggests there is excess unmeasured anion / acid. Keeping it simple, there are only 4 causes: Essentially a state of excess 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 >>

Metabolic Acidosis Evaluation

Metabolic Acidosis Evaluation

A metabolic acidosis is a process which, if uncorrected, would lead to an acidaemia. It is usually associated with a low bicarbonate concentration (or total CO2), but an acidosis may be masked by a co-existing metabolic alkalosis. accumulation of acids (measured, i.e. chloride hyperchloraemic metabolic acidosis] or unmeasured [increased anion gap metabolic acidosis]) renal or gastrointestinal loss of bicarbonate (with absorption of chloride, resulting in hyperchloraemic metabolic acidosis). is usually determined primarily by negatively charged plasma proteins range = 10 to 16 mmol/L (8 to 12 mmol/L if K not included) AG decreases by about 2.5 mmol/L for every decrease in albumin by 10 g/L increased anion gap -> fall in unmeasured cations (Ca, Mg) or increase in unmeasured anions (lactate, ketoacids, formate (methanol), glycolate and oxlate (ethylene glycol)) Toxins methanol, metformin, phenformin, paraldehyde, propylene glycol, pryroglutamic acidosis, iron, isoniazid, ethanol, ethylene glycol, salcylates, solvents GI causes diarrhoea, vomiting, fistulas (pancreatic, ureterostomies, small bowel, ileostomies) Check delta ratio in HAGMA to determine if there is a coexistant NAGMA. osmolar gap can help as a screening test for methanol or ethylene glycol intoxication once alcohol has been excluded (calculated osmolality = 2*Na + Glucose + Urea + ethanol/4.6). urinary pH (inappropriately alkaline for an acidaemia) and electrolytes may facilitate eliciting the specific cause of the renal bicarbonate loss (e.g. renal tubular acidosis). FCICM FACEM BSc(Hons) BHB MBChB MClinEpid(ClinTox) DipPaeds DTM&H GCertClinSim Chris is an Intensivist at the Alfred ICU in Melbourne and is an Adjunct Clinical Associate Professor at Monash University. He is also the Innovation Lead for the Aus Continue reading >>

Salicylate Toxicity - Rebel Em - Emergency Medicine Blog

Salicylate Toxicity - Rebel Em - Emergency Medicine Blog

Boyer, EW. Weilbrecht, KW. Salicylate (aspirin) poisoning in adults. UpToDate. Mar 2018. Link Anderson, RJ et al. Unrecognized adult salicylate intoxication. Ann Intern Med 1976; 85: 745-748. PMID 999110 Goldberg, MA. Barlow, CF. Roth, LJ. The Effects of Carbon Dioxide on the Entry and Accumulation of Drugs in the Central Nervous System. J Pharmacol Exp Ther. (1961) 131: 308-318. PMID 13706469 Hoffman, RS. Howland, MA. Lewin, NA.. Nelson, LS. Goldfrank LR. Goldfrankss Toxicologic Emergencies (10th ed.) New York: McGraw-Hill Education. 516-527. Kuzak N. Brubacher JR. Kennedy JR. Reversal of saliycate induced euglycemic delirium with dextrose. Clinical Toxicology. 45:5; 526-529. PMID 17503260 McCabe, D et al. The association of hemodialysis and survival in intubated salicylate-poisoned patients. Am J Emerg Med 2017; 35: 899-903. PMID 28438446 Temple AR. Acute and Chronic Effects of Aspirin Toxicity and Their Treatment. Arch Intern Med 1981; 141: 364-369. PMID 7469627 Thurston JH et al. Reduced brain glucose with normal plasma glucose in salicylate poisoning. J Clin Invest. 1970: 49 (11); 2139-45. PMID 4319971 Stolbach, AI. Hoffman, RS. Nelson, LS. Mechanical Ventilation Was Associated with Acidemia in a Case Series of Salicylate-poisoned Patients. Soc Acad Emerg Med 2008; 866-869. PMID 18821862 Mosier JM et al. The physiologically difficult airway. West J Emerg Med 2015; 16(7): 1109-17. PMID: 26759664 Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie ) and Anand Swaminathan, MD (Twitter: @EMSwami ) The following two tabs change content below. Continue reading >>

The Interpretation Of Arterial Blood Gases

The Interpretation Of Arterial Blood Gases

The interpretation of arterial blood gases The interpretation of arterial blood gases Aust Prescr 2010;33:124-91 Aug 2010DOI: 10.18773/austprescr.2010.059 Arterial blood gas analysis is used to measure the pH and the partial pressures of oxygen and carbon dioxide in arterial blood. The investigation is relatively easy to perform and yields information that can guide the management of acute and chronic illnesses.This information indicates a patient's acid-base balance, the effectiveness of their gas exchange and the state of their ventilatory control. Interpretation of an arterial blood gas result should not be done without considering the clinical findings.The results change as the body compensates for the underlying problem. Factors relating to sampling technique, specimen processing and environment may also influence the results. Arterial blood gas analysis is a common investigation in emergency departments and intensive care units for monitoring patients with acute respiratory failure. It also has some application in general practice, such as assessing the need for domiciliary oxygen therapy in patients with chronic obstructive pulmonary disease. An arterial blood gas result can help in the assessment of a patient's gas exchange, ventilatory control and acidbase balance. However, the investigation does not give a diagnosis and should not be used as a screening test. It is imperative that the results are considered in the context of the patient's symptoms. While non-invasive monitoring of pulmonary function, such as pulse oximetry, is simple, effective and increasingly widely used, pulse oximetry is no substitute for arterial blood gas analysis. Pulse oximetry is solely a measure of oxygen saturation and gives no indication about blood pH, carbon dioxide or bicarbona Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

OVERVIEW a metabolic acidosis is an abnormal primary process or condition leading to an increase in fixed acids in the blood -> resulting in a fall in arterial plasma bicarbonate CAUSES pathophysiological mechanism: (i) A gain of strong acid (ii) A loss of base the gain of strong acid may be endogenous (eg ketoacids from lipid metabolism) or exogenous (NH4Cl infusion). bicarbonate loss may occur via the bowel (diarrhoea, small bowel fistulas) or via the kidneys (carbonic anhydrase inhibitors, renal tubular acidosis). CLASSIFICATION high anion gap Lactate Toxins – methanol, metformin, phenformin, paraldehyde, propylene glycol, pyroglutamic acidosis, iron, isoniazid, ethanol, ethylene glycol, salicylates, solvents Ketones Renal Normal anion gap Chloride Acetazolamide and Addisons GI causes – diarrhoea, vomiting, fistulas (pancreatic, ureterostomies, small bowel, ileostomies) Extras – RTA MAINTENANCE the disorder is maintained as long as the primary cause persists. in many cases the acid-base disturbance tends to increase in severity while the problem causing it persists though this is not absolute. EFFECTS Respiratory Effects hyperventilation (Kussmaul respirations) – this is the compensatory response shift of oxyhaemoglobin dissociation curve (ODC) to the right – due to the acidosis occurs rapidly decreased 2,3 DPG levels in red cells (shifting the ODC back to the left) -> after 6 hours of acidosis, the red cell levels of 2,3 DPG have declined enough to shift the oxygen dissociation curve (ODC) back to normal. Cardiovascular Effects depression of myocardial contractility sympathetic overactivity resistance to the effects of catecholamines peripheral arteriolar vasodilatation venoconstriction of peripheral veins vasoconstriction of pulmonary arteries (increased Continue reading >>

Acid-base Interpretation

Acid-base Interpretation

1. pH acidaemia or alkalaemia net deviation from normal indicates presence of an acidosis or alkalosis 2. Assess the pattern each of the simple disorders produce predictable changes in either PCO2 or HCO3- 3. Look for associated clues certain conditions produce certain changes in biochemistry HCO3 will change for a 10mmHg change in PaCO2 (1-2-HCO3-4-5 rule) Respiratory Acidosis 1 (acute) -> 4 (chronic) Respiratory Alkalosis 2(acute) -> 5 (chronic) Metabolic Acidosis the 1.5 + 8 Rule (Winters Rule) -> expected PaCO2 at max compensation = 1.5 x HCO3- + 8 Metabolic Alkalosis the Point Seven plus Twenty Rule -> expected pCO2 = 0.7 [HCO3] + 20 5. Other Indices in the Assessment of a Metabolic Acidosis HAGMA look for lactate, calculate Delta ratio, Stewart Equation NAGMA calculate Urinary anion gap, Steward Equation anaerobic muscular activity (sprinting, generalised convulsions) tissue hypoperfusion (shock, cardiac arrest, regional hypoperfusion -> mesenteric ischaemia) reduced tissue oxygen delivery (hypoxaemia, anaemia) or utilisation (CO poisoning) Type B No Evidence of Inadequate Tissue Oxygen Delivery TIPS: thiamine deficiency, infection, pancreatitis, short bowel syndrome FAILURES: hepatic, renal, diabetic failures ethanol intoxication in chronic alcoholics B3: associated with inborn errors of metabolism congenital forms of lactic acidosis with various enzyme defects (eg pyruvate dehydrogenase deficiency) the normal anion gap depends on serum phosphate and serum albumin the normal AG = 0.2 x [albumin] (g/L) + 1.5 x [phosphate] (mmol/L) Can be more simply calculated as (Na+) (Cl- + HCO3-) Causes of an High Anion Gap Metabolic Acidosis (HAGMA) accumulation of organic acids or impaired H+ excretion Toxins methanol, metformin, penformin, paraldehyde, propylene glycol, pyr Continue reading >>

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