Potassium Shift In Dka

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Diabetic Ketoacidosis Nclex Review

NCLEX review on Diabetic Ketoacidosis for nursing lecture exams and the NCLEX exam. DKA is a life-threatening condition of diabetes mellitus. It is important to know the differences between diabetic ketoacidosis and hyperglycemic hyperosmolar nonketotic syndrome (HHNS) because the two complications affect the diabetic patient. However, there are subtle difference between the two conditions. Don’t forget to take the DKA Quiz. In these notes you will learn about: Key Player of DKA Causes of DKA Signs and Symptoms of DKA Nursing Interventions of DKA Lecture on Diabetic Ketoacidosis Diabetic Ketoacidosis Define: a complication of diabetes mellitus that is life-threatening, if not treated. It is due to the breakdown of fats which turn into ketones because there is no insulin present in the body to take glucose into the cell. Therefore, you will see hyperglycemia and ketosis and acidosis. Key Players of DKA: Glucose: fuels the cells so it can function. However, with DKA there is no insulin present to take the glucose into the cell…so the glucose is not used and the patient will experience hyperglycemia >300 mg/dL. Insulin: helps take glucose into the cell so the body can use it for f Continue reading >>

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  1. nurseprnRN

    The hypokalemia comes when the patient gets treated with insulin, driving the glucose and K+ into the cells. The kidneys can't (and won't) move so much out through urine with the excess glucose to make for hypokalemia.

  2. Esme12

    There can be a brief period of hypoglycemia in the early stages of an elevated blood sugar (polyuria)....but by the time "ketoacidosis" sets in the Serum potassium is elevated but the cellular potassium is depleted (all that shifting that goes on)
    Diabetic ketoacidosis

  3. April2152

    So pretty much what we would observe clinically is hyperkalemia because the osmotic duiresis does not move serum potassium significantly?

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How Iv Insulin Can Kill Your Patient

You have a patient that comes up to your unit with a blood sugar of 952. The labs are sent off and the patient is found to be in severe diabetic ketoacidosis (DKA). The doctor puts in the orders for serial lab work, fluid boluses, electrolyte replacements, and an insulin drip. As a newer nurse, you are familiar with labs, boluses, your replacement protocols, but have never administered insulin through an IV. What nursing interventions do you need to perform to safely care for this patient? How Does Insulin Work? Insulin is a hormone created by the pancreas. It allows your body to use glucose to provide the body's cells with the necessary energy they need. Insulin production from the pancreas is based off of your blood sugar levels. If you are getting hyperglycemic, the pancreas is signaled and insulin is released into the bloodstream. Insulin then signals different cells to absorb the glucose and use it as energy or store it for later use. When insulin facilitates glucose being pulled into a cell, a potassium cation is also pulled from extracellular fluid (meaning the bloodstream) into the intracellular fluid. How does this affect our patients? Initially, patients in DKA have an in Continue reading >>

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  1. hippocampus

    What are the potassium level abnormalities associated with DKA (during diagnosis and treatment.)

  2. ahassan

    During DKA, the total body K is low bcz of osmotic diuresis, BUT the serum k conc. is raised bcz of the lack of insulin action, which allows k to shift out of the cells. So hyperkalemia.
    During treatment, k is shifted into the cells, which may lead to profound hypokalemia n death if not treated, so during therapy you have to adjust KCL conc. depending on blood K levels.

  3. tomymajor

    In DKA--> K level may be high or normal so we dont add k from the start of ttt
    But : In HHNKC---> K level is low from the start so we give k from start of ttt

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Explanation of the association between potassium and Acid base balance in the body.

Potassium Balance In Acid-base Disorders

INTRODUCTION There are important interactions between potassium and acid-base balance that involve both transcellular cation exchanges and alterations in renal function [1]. These changes are most pronounced with metabolic acidosis but can also occur with metabolic alkalosis and, to a lesser degree, respiratory acid-base disorders. INTERNAL POTASSIUM BALANCE Acid-base disturbances cause potassium to shift into and out of cells, a phenomenon called "internal potassium balance" [2]. An often-quoted study found that the plasma potassium concentration will rise by 0.6 mEq/L for every 0.1 unit reduction of the extracellular pH [3]. However, this estimate was based upon only five patients with a variety of disturbances, and the range was very broad (0.2 to 1.7 mEq/L). This variability in the rise or fall of the plasma potassium in response to changes in extracellular pH was confirmed in subsequent studies [2,4]. Metabolic acidosis — In metabolic acidosis, more than one-half of the excess hydrogen ions are buffered in the cells. In this setting, electroneutrality is maintained in part by the movement of intracellular potassium into the extracellular fluid (figure 1). Thus, metabolic aci 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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