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Metabolic Acidosis Treatment Ppt

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In late 2015, Medstar Union Memorial Hospital implemented a "Sepsis Response Team" initiative aimed at early detection and intervention in patients with suspected sepsis syndrome. In this program, patients are automatically identified who meet SIRS (systemic inflammatory response syndrome) prompting the nurse to draw a lactate level. Should the lactate level return out of range, the hospital's "Sepsis Response Team" is notified. and intervene, if necessary, either diagnostically or therapeutically. We are hoping that this program will ultimately translate to lower morbidity and mortality from sepsis syndrome at our institution and our system, Medstar Health. In this talk I review the background that our floor medical-surgical nurses will need to better appreciate the program, utility of lactic acid level determination and the related syndromes of sepsis and SIRS.

Lactic Acidosis Update For Critical Care Clinicians

Lactic Acidosis Update for Critical Care Clinicians Franz Volhard Clinic and Max Delbrck Center for Molecular Medicine, Medical Faculty of the Charit Humboldt University of Berlin, Berlin, Germany. Correspondence to Dr. Friedrich C. Luft, Wiltberg Strasse 50, 13125 Berlin, Germany. Phone: 49-30-9417-2202; Fax: 49-30-9417-2206; E-mail: luft/{at}fvk-berlin.de Abstract. Lactic acidosis is a broad-anion gap metabolic acidosis caused by lactic acid overproduction or underutilization. The quantitative dimensions of these two mechanisms commonly differ by 1 order of magnitude. Overproduction of lactic acid, also termed type A lactic acidosis, occurs when the body must regenerate ATP without oxygen (tissue hypoxia). Circulatory, pulmonary, or hemoglobin transfer disorders are commonly responsible. Overproduction of lactate also occurs with cyanide poisoning or certain malignancies. Underutilization involves removal of lactic acid by oxidation or conversion to glucose. Liver disease, inhibition of gluconeogenesis, pyruvate dehydrogenase (thiamine) deficiency, and uncoupling of oxidative phosphorylation are the most common causes. The kidneys also contribute to lactate removal. Concerns hav Continue reading >>

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  1. bflohockeymom

    I vaguely remember our CDE saying this on diagnosis day #1 but I don't have a container in front of me to check. My daughter's school nurse just called and said she thought she smelled ketones on her breath but she checked and the strip said negative. She's been high all week - we've see maybe 3 readings in the 100s which is very abnormal for her. Thought she was getting sick at first, then we had 3 problems with bubbles in the pump tubing, and now this. Her lunch reading was 298.
    Thanks!

  2. Abby-Dabby-Doo

    The urine strips have an expiration date from when you opened them- due to being exposed to air. It should say it on the side of the bottle.
    Blood strips- the date is on the box, I think the foil wrapper too, but I thought the meter wouldn't take them if they were expired.

  3. frizzyrazzy

    Abby-Dabby-Doo said: ↑
    The urine strips have an expiration date from when you opened them- due to being exposed to air. It should say it on the side of the bottle.
    Blood strips- the date is on the box, I think the foil wrapper too, but I thought the meter wouldn't take them if they were expired. I agree with Lanae. The urine strips if I recall was 6 months after opening (or 3) and the blood ketones simply won't work after expiration. Which ticks me off - on 1/1/08 I tried to use a 12/31/07 strip and I got a big fat error.

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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 Continue reading >>

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  1. * DKA explanation

    * DKA explanation

    Below you will find a terrific explanation of DKA from one of the instructors at Med School Tutors. If you like what you see and may be interested in learning more about one-on-one instruction from MST, then please visit their website at www.medschooltutors.com
    In order to understand how to treat DKA, it is useful to first understand what is going on in the body when DKA develops. First of all, DKA (diabetic ketoacidosis) typically develops when a Type I diabetic does not take his or her insulin for a prolonged period of time. It may also be the presentation for new onset diabetes. Because these patients are insulin deficient, they are not able to take up glucose into their cells. This results in two important consequences: 1)glucose builds up in the blood and causes hyperglycemia and 2)the body's cells are forced to breakdown fat for energy, instead of glucose.
    These are very significant consequences... The hyperglycemia results in an osmotic diuresis, because the proximal tubule of the kidney can't reabsorb all the glucose filtered into the nephron. What is osmotic diuresis? Simply that the hyperglycemia (usually >300) causes the body to excrete lots and lots of water, because the osmotic pull of all the glucose particles prevents the reabsorbtion of water in the collecting duct. This means that patients with DKA are peeing their brains out!! They pee out sodium, potassium, and water.. And are therefore, very very very DEHYDRATED, sodium depleted, and potassium depleted.
    Now for the metabolism end of things... The body cells are forced to metabolize fat for energy rather than glucose. How do they accomplish this? - beta-oxidation of fatty acids. This results in excess production of ketone bodies which deplete available acid buffers. This causes a significant metabolic acidosis, with a high anion gap due to the presence of ketoacids. The acidosis causes potassium to shift from the intracellular space to the extracellular space. This may result in a normal or high serum potassium level. This normal or high potassium level masks what is typically significant potassium depletion because the person was peeing all their potassium out as a result of the uncontrolled hyperglycemia.
    So what are we going to do now? I will give a very brief answer for now, expect people to ask questions in the meantime, and then provide a more thorough approach to treatment in the coming days.
    1)Give the patient tons of normal saline. Why? - because your patient is dehydrated as all hell. They have been peeing out every last drop of water because of their severe uncontrolled hyperglycemia. These patients require liters of fluid to replenish all the fluid they've lost as a result of the osmotic diuresis.
    2)Give them insulin. Why? - NOT because it will lower the blood glucose level, but because it will cause a shift away from fat metabolism and toward glucose metabolism. This will slow the production of ketone bodies which are precipitating the metabolic acidosis. Thus, I will repeat, we give insulin to shift away from fat metabolism and stop the production of ketone bodies.
    3)Give the patient potassium. Why? - As we discussed earlier, the person has been peeing out all of their potassium stores and are overall very potassium depleted, despite having normal or high serum potassium levels to begin with. In addition to being potassium depleted, the insulin you are giving will cause a shift of potassium from the extracellular space to the intracellular space, which will drop the serum potassium. Thus, we give DKA patients potassium way before they become hypokalemic.
    4)Give the patient dextrose. Why? - They insulin you are giving the patient is obviously going to cause the serum glucose to decrease. We give glucose to prevent hypoglycemia as we continue to give insulin.
    How do we know when we are finished treating these patients? - When the anion gap returns to normal.
    That's all for now. Please ask any questions you have. I will be giving more specifics about DKA management in the near future.
    PS: Does anyone know the dangerous consequence of giving DKA patients fluid too rapidly? What are the symptoms this may cause, and what is the pathophysiology behind these symptoms?

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Urine Ammonium, Metabolic Acidosis And Progression Of Chronic Kidney Disease

Urine Ammonium, Metabolic Acidosis and Progression of Chronic Kidney Disease Pourafshar N.a · Pourafshar S.a · Soleimani M.b,c aDepartment of Medicine at University of Virginia, Charlottesville, VA, USA bDepartment of Medicine, University of Cincinnati, Cincinnati, OH, USA cDepartment of Medicine Services, Veterans Medical Center, Cincinnati, OH, USA The metabolism of a typical Western diet generates 50–100 mEq of acid (H+) per day, which must be excreted in the urine for the systemic acid-base to remain in balance. The 2 major mechanisms that are responsible for the renal elimination of daily acid under normal conditions are ammonium (NH4+) excretion and titratable acidity. In the presence of systemic acidosis, ammonium excretion is intensified and becomes the crucial mechanism for the elimination of acid. The impairment in NH4+ excretion is therefore associated with reduced acid excretion, which causes excess accumulation of acid in the body and consequently results in metabolic acidosis. Chronic kidney disease (CKD) is associated with the impairment in acid excretion and precipitation of metabolic acidosis, which has an adverse effect on the progression of CKD. Recent studi Continue reading >>

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  1. chele

    During my last urine sample at hospital they noted ketones in my urine. They never mentioned it, but it's got me worried. I'm seeing midwife on Friday and will do another test, but why on earth are there ketones in my urine??!!
    I ate a sandwich before my sample so it's not due to low carbs. I'm not dieting. Ok I've put no weight on, but haven't lost any either (which I admit to finding weird as I've not exactly been eating healthily)
    What could it be due to? Should I worry?

  2. vicky84

    there was leukocytes in mine on thurs and i dont know what that means either!!

  3. chele

    leukocytes is when ur body is fighting off an infection. You might not even know you have one and could be anything such as your body recoverng from a small cut even.
    Anyone else any help on the ketones?

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