Acid-base (anesthesia Text)
There are four native buffer systems – bicarbonate, hemoglobin, protein, and phosphate systems. Bicarbonate has a pKa of 6.1, which is not ideal. Hemoglobin has histidine residues with a pKa of 6.8. Chemoreceptors in the carotid bodies, aortic arch, and ventral medulla respond to changes in pH/pCO2 in a matter of minutes. The renal response takes much longer. Arterial vs. Venous Gases Venous blood from the dorsum of the hand is moderately arterialized by general anesthesia, and can be used as a substitute for an ABG. pCO2 will only be off by ~ 5 mm Hg, and pH by 0.03 or 0.04 units [Williamson et. al. Anesth Analg 61: 950, 1982]. Confounding variables include air bubbles, heparin (which is acidic), and leukocytes (aka “leukocyte larceny”). VGB/ABG samples should be cooled to minimize leukocyte activity, however when blood is cooled, CO2 solubility increases (less volatile), and thus pCO2 drops. As an example – a sample taken at 37°C and at 7.4 will actually read as a pH of 7.6 if measured at 25°C. Most VBG/ABGs are actually measured at 37°C. A-aDO2 increases with age, as well as with increased FiO2 and vasodilators (which impair hypoxic pulmonary vasoconstriction). In the setting of a shunt, pulse oximetry can be misleading, thus the A-aDO2 should be calculated. If PaO2 is > 150 mm Hg (i.e., Hg saturation is essentially 100%), every 20 mm Hg of A-aDO2 represents 1% shunting of cardiac output. A/a is even better than A-aDO2 because it is independent of FiO2. PaO2/FiO2 is a reasonable alternative, with hypoxia defined as PaO2/FiO2 < 300 (a PaO2/FiO2 < 200 suggests a shunt fraction of 20% or more). Mixed venous blood should have a pO2 of ~ 40 mm Hg. Values < 30 mm Hg suggest hypoxemia, although one must always keep in mind that peripheral shunting and cyanide tox Continue reading >>
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 >>
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Acid-base Disorders
Content currently under development Acid-base disorders are a group of conditions characterized by changes in the concentration of hydrogen ions (H+) or bicarbonate (HCO3-), which lead to changes in the arterial blood pH. These conditions can be categorized as acidoses or alkaloses and have a respiratory or metabolic origin, depending on the cause of the imbalance. Diagnosis is made by arterial blood gas (ABG) interpretation. In the setting of metabolic acidosis, calculation of the anion gap is an important resource to narrow down the possible causes and reach a precise diagnosis. Treatment is based on identifying the underlying cause. Continue reading >>
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Secondary responses to alterations in acid-base status Hypercapnia acidifies body fluids and titrates nonbicarbonate buffers, yielding a small increase in plasma [HCO3]. This secondary hyperbicarbonatemic response is completed within 5 to 10 minutes and remains stable for several hours. Observations in unanesthetized normal humans studied in an environmental chamber (inspired CO2 7 and 10%) reveal a mean [HCO3]/Paco2 slope of 0.1 mEq/L per mmHg; expected [HCO3] = 24 + [(current Paco2 40) 0.1]. 4 An essentially identical slope is obtained in humans in whom respiratory acidosis is induced by endogenous hypercapnia. 5 Sustained hypercapnia causes an additional, larger increase in plasma [HCO3] owing to stimulation of renal acidification. In dogs, a new steady state emerges within 3 to 5 days. 6 , 7 Whether this temporal pattern applies to humans is unknown. In patients, chronic hypercapnia often reflects gradual deterioration in pulmonary function; consequently, the secondary response might keep pace with the slowly rising Paco2 without a perceptible delay. Careful observations of patients with chronic hypercapnia as a result of chronic obstructive pulmonary disease allowed estimation of a mean [HCO3]/Paco2 slope of 0.35 mEq/L per mmHg; expected [HCO3] = 24 + [(current Paco2 40) 0.35]. This slope functions up to a Paco2 of approximately 70 mmHg. Beyond that level, the slope of [HCO3]/Paco2 seems to flatten. 8 , 9 More recently, a substantially larger slope was reported, but the small number of blood gas measurements, one for each of 18 patients, calls into question the validity of the conclusion reached. 10 Hypocapnia alkalinizes body fluids and titrates nonbicarbonate buffers, yielding a decrease in plasma [HCO3]. This secondary hypobicarbonatemic response is completed w Continue reading >>
Metabolic Acidosis & Metabolic Alkalosis
Published by Lambert Morgan Modified over 2 years ago Presentation on theme: "Metabolic acidosis & Metabolic alkalosis" Presentation transcript: 1 Metabolic acidosis & Metabolic alkalosis 3 Primary Change Secondary change Net effect Hco3 Pco2 pH ( H+) Pco2 should by 1.2 mmHg for each mEq plasma Hco3 Inability to excrete dietary acid load Renal failure Renal tubular acidosis type 1 &4 Increased H+ load Lactic acidosis Ketoacidosis Toxin ingestions Increased HCO3 loss diarrhoea 5 Normal anion gap or hyper chloremic acidosis AG = Na+ (Hco3 + Cl ) Normal = 12 4 ( 8 16 ) Measure of unmeasured anion (protiens) Normal anion gap or hyper chloremic acidosis High anion gap 6 Metabolic acidosis Lactic acidosis Ketoacidosis Diarrhoea High anion gap Normal anion gap Lactic acidosis Ketoacidosis Renal failure Toxin ingestions Salicylate Methanol Ethylene glycol Diarrhoea Renal tubular acidosis 7 Clinical features Kussmals respiration (increased depth than rate) Neurologic symptoms: lethargy to coma In severe acidosis (pH< 7.1): Cardiac arrhythmia Reduced cardiac contractility Decreased inotropic response to catecholamines. Chronic acidosis Impaired growth in children Osteomalacia/osteopenia 8 Treatment Treat the underlying cause NaHCO3 therapy: Severe metabolic acidosis (pH<7.1) Chronic acidosis (sodium or potassium citrate) To alkalanise urine in salicylate poisoning 9 NaHCO3 therapy in severe acidosis: pH <7.1 Always treat the pH and not the HCO3 Only one half of bicarbonate deficit to be corrected in initial 12 hrs NaHCO3 dose= desired HCO3 observed HCO3 * 50%of body wt desired HCO3 =12 meq/L in HAG acidosis and meq/L in NAG 10 Example A 24 yr old type 1 diabetic male, weighing aroud 50 Kg presenting with fever, tachypnoea and abd pain to the EMU pH HCO pCo Urine ketones + BP 100 Continue reading >>
Metabolic Acidosis | Washington Manual Of Medical Therapeutics
Washington Manual of Medical Therapeutics Type your tag names separated by a space and hit enter To view the entire topic, please sign in or purchase a subscription . The Washington Manual of Medical Therapeutics helps you diagnose and treat hundreds of medical conditions. Consult clinical recommendations from a resource that has been trusted on the wards for 50+ years. Explore these free sample topics: -- The first section of this topic is shown below -- The causes of a metabolic acidosis can be divided into those that cause an elevated AG and those with a normal AG. Many of the causes seen in clinical practice can be found in Table 12-3 . AG acidosis results from exposure to acids, which contribute an UA to the ECF. Common causes are DKA, lactic acidosis, and toxic alcohol ingestions. NonAG acidosis can result from the loss of from the GI tract. Renal causes due to renal excretion of or disorders of renal acid handling are referred to collectively as RTAs. loss occurs most commonly in the setting of severe diarrhea. The three forms of RTA correlate with the three mechanisms that facilitate renal acid handling: proximal bicarbonate reabsorption, distal H+ secretion, and generation of NH3, the principle urinary buffer. Urinary buffers reduce the concentration of free H+ in the filtrate, thus attenuating the back leak of H+, which occurs at low urinary pH. Proximal (type 2) RTA is caused by impaired proximal tubular reabsorption. Causes include inherited mutations (cystinosis), heavy metals, drugs (tenofovir, ifosfamide, carbonic anhydrase inhibitors), and multiple myeloma and other monoclonal gammopathies. Distal (type 1) RTA results from impaired distal H+ secretion. This may occur because of impairment in H+ secretion, as seen with a variety of autoimmune (Sjgren syn Continue reading >>
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 >>
Respiratory Acidosis
Respiratory acidosis is an acid-base balance disturbance due to alveolar hypoventilation. Production of carbon dioxide occurs rapidly and failure of ventilation promptly increases the partial pressure of arterial carbon dioxide (PaCO2). [ 1 ] The normal reference range for PaCO2 is 35-45 mm Hg. Alveolar hypoventilation leads to an increased PaCO2 (ie, hypercapnia). The increase in PaCO2, in turn, decreases the bicarbonate (HCO3)/PaCO2 ratio, thereby decreasing the pH. Hypercapnia and respiratory acidosis ensue when impairment in ventilation occurs and the removal of carbon dioxide by the respiratory system is less than the production of carbon dioxide in the tissues. Lung diseases that cause abnormalities in alveolar gas exchange do not typically result in alveolar hypoventilation. Often these diseases stimulate ventilation and hypocapnia due to reflex receptors and hypoxia. Hypercapnia typically occurs late in the disease process with severe pulmonary disease or when respiratory muscles fatigue. (See also Pediatric Respiratory Acidosis , Metabolic Acidosis , and Pediatric Metabolic Acidosis .) Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (ie, >45 mm Hg) with an accompanying acidemia (ie, pH < 7.35). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate levels (ie, >30 mEq/L). Acute respiratory acidosis is present when an abrupt failure of ventilation occurs. This failure in ventilation may result from depression of the central respiratory center by one or another of the following: Central nervous system disease or drug-induced r Continue reading >>
Metabolic Alkalosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition
(Video) Overview of Buffering and the Henderson-Hasselbalch Equation By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincents Ascension Health, Birmingham Metabolic alkalosis is primary increase in bicarbonate (HCO3) with or without compensatory increase in carbon dioxide partial pressure (Pco2); pH may be high or nearly normal. Common causes include prolonged vomiting, hypovolemia, diuretic use, and hypokalemia. Renal impairment of HCO3 excretion must be present to sustain alkalosis. Symptoms and signs in severe cases include headache, lethargy, and tetany. Diagnosis is clinical and with arterial blood gas and serum electrolyte measurement. The underlying condition is treated; oral or IV acetazolamide or hydrochloric acid is sometimes indicated. Metabolic alkalosis is bicarbonate (HCO3) accumulation due to Intracellular shift of hydrogen ion (H+as occurs in hypokalemia ) Regardless of initial cause, persistence of metabolic alkalosis indicates that the kidneys have increased their HCO3 reabsorption, because HCO3 is normally freely filtered by the kidneys and hence excreted. Volume depletion and hypokalemia are the most common stimuli for increased HCO3 reabsorption, but any condition that elevates aldosterone or mineralocorticoids (which enhance sodium [Na] reabsorption and potassium [K] and hydrogen ion [H+] excretion) can elevate HCO3. Thus, hypokalemia is both a cause and a frequent consequence of metabolic alkalosis. The most common causes of metabolic alkalosis are Volume depletion (particularly when involving loss of gastric acid and chloride [Cl] due to recurrent vomiting or nasogastric suction) Among other causes (see Table: Causes of Metabolic Alkalosis ) are disorders that cause Continue reading >>
Acid Base Homeostasis + Imbalance (ppt)
presence of condition that tends to decrease pH of blood making it more acidic presence of factor that increases pH of blood above normal, making it more alkaline -relative excess of any acid except carbonic acid -combo of increase in acid and decrease in base results in decrease of normal 20:1 ratio of HCO3- to H2CO3 decreases normal ratio of bicarbonate to carbonic acid because bicarbonate ions are used up in buffering the excess acid -caloric + glucose intake is insufficient -body begins to use fat stores for energy -ketoacids accumulate in blood causing metabolic acidosis other examples of increase in acid in (metabolic acidosis) -ketoacidosis (diabetes mellitus, starvation, alocoholism) compensatory response to metabolic acidosis hyperventilation as a compensatory response to metabolic acidosis -low blood pH stimulates peripheral chemoreceptors -ventilatory neurons respond to increase rate + depth of respiration -results in increased excretion by lungs of carbonic acid (CO2 + H2O) results of compensatory response in metabolic acidosis -does change ratio of bicarbonate ions to carbonic acid -decreased bicarbonate concentration (primary disorder) -decreased PaCO2 (compensation; normal in primary disorder) -decreased (somewhat low) or even normal pH depending on degree of compensation which for the following would be associated w. metabolic acidosis c. prolonged vomiting or gastric suctioning a. central nervous system depression --> coma, stupor, lethargy, confusion b. increased serum bicarbonate levels --> no; see a decrease in bicarbonate (base) which results in acidosis c. prolonged vomiting or gastric suctioning --> no, this would deplete the body of acids leadings to alkalosis d. ph greater than 7.40 --> no, you would expect a decrease in pH due to decrease in b Continue reading >>
Paediatric Acid-base Disorders: A Case-based Review Of Procedures And Pitfalls
Paediatric acid-base disorders: A case-based review of procedures and pitfalls J Bryan Carmody , MD and Victoria F Norwood , MD Department of Pediatrics, Division of Pediatric Nephrology, University of Virginia, Charlottesville, Virginia, USA Correspondence: Dr J Bryan Carmody, Department of Pediatrics, Division of Pediatric Neprhology, University of Virginia, PO Box 800386, Charlottesville, Virginia 22903, USA. Telephone 434-924-2096, e-mail ude.ainigriv.ccm.liamcsh@d5cbj , moc.xobnur@ydomracbj Copyright 2013 Pulsus Group Inc. All rights reserved Acid-base disorders occur frequently in paediatric patients. Despite the perception that their analysis is complex and difficult, a straightforward set of rules is sufficient to interpret even the most complex disorders provided certain pitfalls are avoided. Using a case-based approach, the present article reviews the fundamental concepts of acid-base analysis and highlights common mistakes and oversights. Specific topics include the proper identification of the primary disorder; distinguishing compensatory changes from additional primary disorders; use of the albumin-corrected anion gap to generate a differential diagnosis for patients with metabolic acidosis; screening for mixed disorders with the delta-delta formula; recognizing the limits of compensation; use of the anion gap to identify hidden acidosis; and the importance of using information from the history and physical examination to identify the specific cause of a patients acid-base disturbance. Keywords: Acid-base equilibrium, Acid-base imbalances, Acidosis, Alkolosis, Blood Les troubles de lquilibre acido-basique sont frquents chez les patients dge pdiatrique. Mme si on les croit difficiles et complexes analyser, des rgles simples suffsent pour interprter mme les Continue reading >>
Metabolic Acidosis Nclex Review Notes
Are you studying metabolic acidosis and need to know a mnemonic on how to remember the causes? This article will give you a clever mnemonic and simplify the signs and symptoms and nursing interventions on how to remember metabolic acidosis for nursing lecture exams and NCLEX. In addition, you will learn how to differentiate metabolic acidosis from metabolic alkalosis. Don’t forget to take the metabolic acidosis and metabolic alkalosis quiz. This article will cover: Metabolic acidosis simplified Lab values expected with metabolic acidosis Causes of metabolic acidosis Signs and symptoms of metabolic acidosis Nursing interventions for metabolic acidosis Lecture on Metabolic Acidosis Metabolic Acidosis Metabolic Acidosis in Simple Terms: a metabolic problem due to the buildup of acid in the body fluids which affects the bicarbonate (HCO3 levels) either from: increased acid production (ex: DKA where ketones (acids) increase in the body which decreases bicarbonate) decreased acid excretion (ex: renal failure where there is high amount of waste left in the body which causes the acids to increase and bicarb can’t control imbalance) loss of too much bicarb (diarrhea) When this acidic phenomena is taking place in the body other systems will try to compensate to increase the bicarb back to normal. One system that tries to compensate is the respiratory system. In order to compensate, the respiratory system will cause the body to hyperventilate by increasing breathing through Kussmaul’s respirations. Kussmaul respirations are deep, rapid breathes. The body hopes this will help expel CO2 (an acid) which will “hopefully” increase the pH back to normal. Lab values expected in Metabolic Acidosis: HCO3: decreased <22 Blood pH: decreased <7.35 CO2: <35 or normal (may be normal b Continue reading >>
Metabolic Acidosis: Causes, Symptoms, And Treatment
The Terrible Effects of Acid Acid corrosion is a well-known fact. Acid rain can peel the paint off of a car. Acidifying ocean water bleaches and destroys coral reefs. Acid can burn a giant hole through metal. It can also burn holes, called cavities, into your teeth. I think I've made my point. Acid, regardless of where it's at, is going to hurt. And when your body is full of acid, then it's going to destroy your fragile, soft, internal organs even more quickly than it can destroy your bony teeth and chunks of thick metal. What Is Metabolic Acidosis? The condition that fills your body with proportionately too much acid is known as metabolic acidosis. Metabolic acidosis refers to a physiological state characterized by an increase in the amount of acid produced or ingested by the body, the decreased renal excretion of acid, or bicarbonate loss from the body. Metabolism is a word that refers to a set of biochemical processes within your body that produce energy and sustain life. If these processes go haywire, due to disease, then they can cause an excess production of hydrogen (H+) ions. These ions are acidic, and therefore the level of acidity in your body increases, leading to acidemia, an abnormally low pH of the blood, <7.35. The pH of the blood mimics the overall physiological state in the body. In short, a metabolic process is like a power plant producing energy. If a nuclear power plant goes haywire for any reason, then we know what the consequences will be: uncontrolled and excessive nuclear energetic reactions leading to the leakage of large amounts of radioactive material out into the environment. In our body, this radioactive material is acid (or hydrogen ions). Acidemia can also occur if the kidneys are sick and they do not excrete enough hydrogen ions out of th Continue reading >>
Effects Of Respiratory Alkalosis And Acidosis On Myocardial Blood Flow And Metabolism In Patients With Coronary Artery Disease | Anesthesiology | Asa Publications
Effects of Respiratory Alkalosis and Acidosis on Myocardial Blood Flow and Metabolism in Patients with Coronary Artery Disease (Weyland, Rieke) Associate Professor of Anesthesiology. (Stephan, Sonntag) Professor of Anesthesiology. Effects of Respiratory Alkalosis and Acidosis on Myocardial Blood Flow and Metabolism in Patients with Coronary Artery Disease Anesthesiology 10 1998, Vol.89, 831-837. doi: Anesthesiology 10 1998, Vol.89, 831-837. doi: Stephan Kazmaier, Andreas Weyland, Wolfgang Buhre, Heidrun Stephan, Horst Rieke, Klaus Filoda, Hans Sonntag; Effects of Respiratory Alkalosis and Acidosis on Myocardial Blood Flow and Metabolism in Patients with Coronary Artery Disease . Anesthesiology 1998;89(4):831-837. 2018 American Society of Anesthesiologists Effects of Respiratory Alkalosis and Acidosis on Myocardial Blood Flow and Metabolism in Patients with Coronary Artery Disease 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 ALTHOUGH unintended or deliberate variation of the arterial carbon dioxide partial pressure (PaCO2) is common in anesthetic practice, little is known about the myocardial consequences of respiratory alkalosis and acidosis in humans. Previous experimental studies have shown inconsistent results with respect to the effects of PaCO2on myocardial blood flow (MBF), myocardial metabolism, and global hemodynamics. This may have been caused in part by differences in the experimental design of the investigations. [1-6] Although most studies have shown that hypercapnia augments MBF above metabolic demands, [3,7-9] the results with respect to the effects of hypocapnia vary. [3,4] Furthermore, it seems questionable to transfer conclusions from experiment Continue reading >>
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Metabolic Acidosis And Alkalosis.ppt
LEARNING OBJECTIVESNORMAL VALUES OF ABGTYPES AND CAUSES OF METABOLIC ACIDOSIS AND METABOLIC ALKALOSISDISODERS WITH HIGH AND LOW ANIONIC GAPDIFFERENT CASE SENARIO Normal valuesFrom serum (venous) blood:CO2 (bicarb) 22-32 mmol/LNa 135-146 mmol/LCl 98-111 mmol/LFrom ABG:pH 7.35-7.45pCO2 35-45Bicarb 21-29 Metabolic AcidosisHCO3- excretion is controlled by the kidneyH+ excretion is controlled by the kidneyOne H+ buffers one HCO3-So, an increase in H+ can cause a decrease in HCO3- Metabolic AcidosisGain of H+ Loss of HCO3-(bicarb) Causes of metabolic acidosis due to gain of acid Endogenous hydrogen ion production: ketoacidosis lactic acidosis salicylate overdoseMetabolism of toxins methanol ethylene glycolDecreased renal excretion uremia renal tubular acidosis (type 1) distal Causes of metabolic acidosis due to loss of bicarb--Renal tubular acidosis type II (proximal)--GI loss (diarrhea) Metabolic AcidosisMetabolic acidosis can be characterized based on anion gapHigh anion gap >20Normal anion gap 7-15 meq/L AG=Na (Cl + HCO3-) Diff Dx of elevated anion gap acidosisMethanol intoxication (denatured alcohol)Uremic acidosisDiabetic ketoacidosisParaldehyde intoxication/alcohol intoxicationI INH, infectionLactic acidosisEthylene glycol intoxicationSalicylate intoxication Elevated anion gap acidosisMethanol intoxicationIngested methanol is converted in the body to formic acid leading to metabolic acidosis and high anion gapAlso will have increased osmolal gapAntifreeze, de-icing solutions, cleaners, solventsSymptoms include optic neuritis, blindness, pancreatitisTreatment:Give ethanol IV to stop methanol conversion to formic acidFomepizoleDialysisbicarbonate Elevated anion gap acidosisUremic acidosisOccurs in severe renal failure with GFR <20%Kidneys unable to excrete H+ Treatment:d Continue reading >>
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