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    1. The patient was admitted to the ED after cardiac arrest with a potassium level of 9. He was given insulin, beta-agonists, and calcium to treat his hyperkalemia. 2. Further workup found an acidosis and potassium pills in his stomach. He underwent dialysis to control his potassium level and stabilize his condition. 3. Kayexalate was used to bind potassium in his digestive tract to prevent further absorption, while dialysis filtered his blood to regulate the elevated potassium.

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    1. The patient was admitted to the ED after cardiac arrest with a potassium level of 9. He was given insulin, beta-agonists, and calcium to treat his hyperkalemia. 2. Further workup found an acidosis and potassium pills in his stomach. He underwent dialysis to control his potassium level and stabilize his condition. 3. Kayexalate was used to bind potassium in his digestive tract to prevent further absorption, while dialysis filtered his blood to regulate the elevated potassium.

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    64 views4 pages

    RLEFandECS Garlitos Roanne

    Uploaded by

    Paul Jackson
    1. The patient was admitted to the ED after cardiac arrest with a potassium level of 9. He was given insulin, beta-agonists, and calcium to treat his hyperkalemia. 2. Further workup found an acidosis and potassium pills in his stomach. He underwent dialysis to control his potassium level and stabilize his condition. 3. Kayexalate was used to bind potassium in his digestive tract to prevent further absorption, while dialysis filtered his blood to regulate the elevated potassium.

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    of 4

    RLE: Managing Electrolyte Imbalances: A Case of Self-Induced Imbalance

    Perfect Score Score


    Questions and Rationale 21

    This is the case of a 38-year-old male that was transferred to an emergency department (ED) from an another
    hospital status post cardiac arrest. The patient was an inmate at a district prison who was found
    unresponsive in his cell. Emergency Medical Services (EMS) was called for medical support. Minimal health
    information was provided by the prison. The patient was found by EMS to be in ventricular tachycardia with a
    palpable pulse and was intubated on the scene. The patient was given 150 mg of amiodarone, and
    transportation to an outside facility was initiated. On laboratory evaluation at the outside hospital, the
    patient was noted to have a potassium level of 9. Treatment of the patient's hyperkalemia with insulin, beta-
    agonists, and calcium was initiated. After initial resuscitation, the patient was transported to our ED. While en
    route, the patient experienced an episode of pulseless ventricular tachycardia, requiring two episodes of
    cardioversion. Return of spontaneous circulation was achieved prior to ED arrival.

    Questions:
    1. The patient’s potassium level is: Encircle one (1 pt)
    a. High
    b. Low
    2. Why is the patient given (2 pts each, provided references)

    a. Insulin:
    Insulin is given because much like glucose, it encourages potassium movement back
    into the cells from the extracellular space, thus decreasing the potassium levels
    needed since the patient has hyperkalemia.

    Stoppler, M. Hyperkalemia (High Blood Potassium). Retrieved from:


    https://www.medicinenet.com/hyperkalemia/article.htm

    Li,T. & Vijayan, A. (2014, June). Insulin for the treatment of hyperkalemia: a double-edged sword?
    Retrieved from:
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4377764/#:~:text=Insulin%20shifts%20potassi
    um%20into%20cells,serum%20potassium%20levels%20%5B16%5D

    b. Beta-agonist
    Beta agonists activates membrane-bound Na/K-ATPase and cause potassium levels shift into cell. Too
    much use of this medication if not being controlled will lead to hypokalemia.

    Mushiyakh, Y. et al. (2011). Treatment and pathogenesis of acute hyperkalemia. Retrieved from:
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3714047/
    Ng, K. & Lee, C. (2017, February 16). Updated Treatment Options in the Management of
    Hyperkalemia. Retrieved from: https://www.uspharmacist.com/article/updated-treatment-
    options-in-the-management-of-hyperkalemia

    c. Calcium
    Without lowering potassium level, calcium directly antagonizes the myocardial effects
    of hyperkalemia. It antagonizes the cardiotoxicity of hyperkalemia by stabilizing the
    cardiac cell membrane against undesirable depolarization. This is done by reducing
    the threshold potential of cardiac myocytes, thereby restoring the normal gradient of
    the hyperkalemia-distorted resting membrane potential. Calcium protects the
    myocardium and cardiac membranes from hyperkalemia's deleterious effects.

    Ledere, E. (2020, April 09). Hyperkalemia Medication. Retrieved from:


    https://emedicine.medscape.com/article/240903-medication
    Weisberg, L. Management of severe hyperkalemia. Retrieved from: https://emcrit.org/wp-
    content/uploads/Management_of_severe_hyperkalemia.18.pdf

    In the ED, vitals were as follows: blood pressure 90/50, heart rate 143 beats per minute, respiratory rate 13
    breaths per minute, oxygen (O2) saturation 99%, temperature 35.4 Celsius (C). An electrocardiogram (ECG)
    was performed, which documented ventricular tachycardia at a rate of 140 without ST segment or T wave
    changes. On exam, the patient was noted to be intubated. Head, ears, eyes, nose, and throat (HEENT) exam
    revealed 3 millimeter (mm) pupils that were sluggishly reactive to light and equal bilaterally and an
    endotracheal tube at 25 centimeters (cm) at the teeth. The remainder of the HEENT exam was unremarkable.
    Neck exam revealed a cervical collar in place with no cervical spine step-off noted. Cardiovascular exam
    revealed a heart rate of 140 beats per minute with palpable distal pulses. Lungs were clear to auscultation
    bilaterally. Abdomen was soft with good bowel sounds and no evidence of distension. On neurological exam,
    the patient was noted to be sedated with a Glasgow coma scale (GCS) of 3T.

    3. Is the ECG result expected of his case? Encircle one (1 pt)


    a. Yes
    b. No
    4. What is the rationale behind your answer? (2pt, provided references)
    Since ventricular tachycardia is expected in the case of the patient, the T-wave should look tall
    "tented" or peaked.

    Parham, W. (2006). Hyperkalemia Revisited. Retrieved from:


    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1413606/

    Lederer, E. (2020, April 09). What do ECG findings indicate in hyperkalemia (high serum potassium
    level). Retrieved from: https://www.medscape.com/answers/240903-11014/what-do-ecg-
    findings-indicate-in-hyperkalemia-high-serum-potassium-level

    Sims, D. &Sperling, L. (2005, May 17). ST-Segment Elevation Resulting From Hyperkalemia. Retrieved
    from: https://www.ahajournals.org/doi/10.1161/01.CIR.0000165127.41028.D1
    The patient had blood sent to the lab for multiple studies. The patient's complete blood count (CBC)
    revealed a white blood cell count of 23.6 thou/cu mm, a hemoglobin of 14.7 g/dL, a hematocrit of
    45.5%, her and a platelet count of 181 thou/cu mm. His basic metabolic panel revealed a sodium of 143 
    mmol/L, a potassium of 8.7 mmol/L, a chloride of 120 mmol/L, a bicarbonate of 16 mmol/L, a BUN of 22 
    mg/dL, a creatinine of 1.06 mg/dL, and a glucose of 191 mg/dL. Arterial blood gas revealed a pH of 7.06,
    pCO2 of 58 mmHg, and pO2 of 77 mmHg. Cardiac markers and urinalysis were both unremarkable. A
    urine drug screen was positive for benzodiazepines.

    5. Interpret that patient’s ABG result: (5 pts)

    It’s Mixed Acidosis because partial pressure of carbon dioxide is much higher than
    concentration of hydrogen carbonate in the blood.

    pH - 7.06 – Acidosis
    pCO2- 58mmHg – Acidosis
    HCO3- 16mmol/L - Acidosis

    6. How is this related to the patient’s case? (2 pts, provided references)


    Acidosis induces potassium, in exchange for hydrogen ions, to pass from cells to extracellular
    fluid (plasma). To elaborate, it allows the movement of potassium from the intracellular
    compartment to the extracellular compartment, resulting in a high amount of potassium that
    causes the patient to suffer from hyperkalemia.

    Higging, C. (2013, October). On the relationship between potassium and acid-base balance. Retrieved
    from: https://acutecaretesting.org/en/journal-scans/on-the-relationship-between-potassium-
    and-acid-base-
    balance#:~:text=A%20frequently%20cited%20mechanism%20for,of%20potassium%20and%20h
    ydrogen%20ions.

    Harris, A. et al. Mechanism of Hyperkalemia-Induced-Metabolic Acidosis. Retrieved from:


    https://www.researchgate.net/publication/323399425_Mechanism_of_Hyperkalemia-
    Induced_Metabolic_Acidosis
    The patient's emergency department management began with initial stabilization. Due to his persistent
    ventricular tachycardia, the patient was given another bolus of amiodarone upon arrival and a subsequent
    amiodarone infusion was started. Due to low mean arterial pressures, two liter of normal saline was given
    intravenously, a right subclavian central venous line was placed, and a left radial arterial line was placed. A
    levophed drip was started at 0.1 mcg/kg/min and titrated to maintain a mean arterial pressure (MAP) of 65
    for pressure support. Treatment for hyperkalemia was readministered concurrently, consisting of insulin,
    beta-agonists and kayexalate. Chest X-ray revealed clear lungs with radio paque capsules in the fundus of the
    stomach. Over the next thirty minutes, the patient's rhythm converted to normal sinus rhythm and slowed to
    around 70 beats per minute. Repeat potassium lab draw revealed persistently elevated potassium level of 8.3 
    mmol/L, and hyperkalemia treatment was repeated. At this point, nephrology was consulted for emergent
    dialysis, and the medical intensive care unit (MICU) was notified for admission. We later found out, from the
    MICU team, that the patient had an esophagogastroduodenoscopy (EGD) performed to remove the unknown
    pills from the patient's stomach, which were found to be potassium chloride pills. After removal of the pills
    and multiple episodes of dialysis, the patient stabilized and was weaned from pressure and ventilator support.
    The patient's leukocytosis was believed to be a stress response as the MICU team was never able to
    determine a source of infection; however, the patient remained on-broad spectrum intravenous antibiotics
    over the course of his stay.

    7. What is the role of kayexalate? (2 pts, provided references)

    In the digestive tract, it binds to potassium, which allows the body not to consume too much
    potassium. This is a standard treatment for hyperkalemia or elevated blood potassium levels.

    Unknown. Retrieved from: https://www.webmd.com/drugs/2/drug-3731/kayexalate-


    oral/details#:~:text=This%20medication%20is%20used%20to,get%20rid%20of%20extra
    %20potassium.
    Unknown. Retrieved from: https://chealth.canoe.com/drug/getdrug/kayexalate

    8. What is the role of dialysis in this case? (2 pts, provided references)

    The patient's blood is filtered and most importantly, the elevated potassium is regulated in
    order for the patient to return to normal levels. Dialysis is performed when a person has
    kidney issues, because pharmacological treatment alone is not sufficient to safely decrease
    the level of potassium.

    Garth, D. (2019, August 06). What is the role of dialysis in the treatment of hyperkalemia (high serum
    potassium level). Retrieved from: https://pubmed.ncbi.nlm.nih.gov/17897250/

    Putch, N. & Allon, M. (2007). Management of hyperkalemia in dialysis patients. Retrieved from:
    https://pubmed.ncbi.nlm.nih.gov/17897250/#:~:text=Abstract,used%20to%20stabilize%20the%20myoc
    ardium.

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