mnemonic for lyte imbalances?

  1. Help....I can't keep all of the electrolyte imbalances straight! I have my final on Monday and was wondering if anyone had a technique or mnemonic to help with this (such as hyper/hypo magensemia, calcemia, natremia...) and all the signs/symptoms the patient demonstrates ... they can be so confusing because there are several for each imbalance.

    Thank you!!!

    ~J
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  2. 5 Comments

  3. by   VickyRN
    Here are a few:

    Hypernatremia:
    Think of "SALT"
    -Skin flushed
    -Agitation
    -Low-grade fever
    -Thirst

    Reciprocal relationship between calcium and phosphorus:
    INCREASED Ca2+ = DECREASED PO43-
    -Increasing serum calcium levels decreases phosphate levels
    -Decreasing serum calcium increases phosphate

    Chvostek's and Trousseau's signs; Tetany, irritability, and seizures:
    Hypocalcemia
    Hypomagnesemia
    Hyperphosphatemia

    Electrolyte imbalances which can potentiate dig toxicity:
    Hypokalemia
    Hypomagnesemia
    Hypercalcemia

    Electrolyte imbalances which can cause dysrhythmias:
    Hypo/ hypokalemia
    Hypomagnesemia
    Hypocalcemia

    Both HYPO and HYPER natremia can cause mental confusion, seizures, and coma

    Both HYPO and HYPER kalemia can cause cardiac dysrhythmias progressing to ventricular fibrillation and asystole. Think "cardiac" with both. Hyperkalemia is the most deadly of all electrolyte imbalances.

    Good book:
    ttp://www.elsevier.com/wps/find/bookdescription.cws_home/707132/description#description
  4. by   VickyRN
    A few others (from looking at my notes):

    Almost all of the osmotic pressure in extracellular fluids (ECF) is due to:
    Na+ and Cl-

    Important functions of sodium in the body.
    Maintains ECF osmolarity (fluid balance)
    Maintains ECF electroneutrality
    Conducts action potentials in nerve/ muscle tissue (initiates skeletal muscle contractions)
    Acid-base balance (sodium bicarbonate)

    A. The renin-angiotensin-aldosterone mechanism:
    Save Na+
    B. ANP (atrial natriuretic peptide):
    Lose Na+
    C. ADH (antidiuretic hormone):
    No effect on Na+ (will cause dilutional hyponatremia, however)

    ADH think WATER (PURE water without sodium, being retained):
    ADH stimulates kidney tubule cells to become more permeable to water. In other words, ADH tells kidneys to "save the water!"
    ADH increases blood volume (blood becomes "less thick") as urine output is decreased?.
    ADH increases the permeability of the membrane to water and enhances free water reabsorption. Causes more water to be reabsorbed and returned to the circulation, making the blood more dilute (reduced osmolarity of the blood). The urine will then be more concentrated.

    The name antidiuretic hormone (ADH) indicates that its effects are opposite those of diuretics.

    Increased serum chloride equals increased serum sodium.

    Increased serum chloride equals decreased serum bicarbonate (HCO3-).

    Both hyponatremia and hypernatremia can cause:
    LOC changes, confusion, seizures, coma

    Electrolyte imbalances mainly the result of renal failure:
    Hyperkalemia, hypermagnesemia, hypocalcemia, hyperphosphatemia

    Both hypokalemia and hyperkalemia can cause:
    Skeletal muscle weakness, paralysis, lethal cardiac dysrhythmias, cardiac arrest

    Medications contributing to hypokalemia:
    Loop and thiazide diuretics (Lasix, Edecrin, HCTZ), laxatives and enemas (GoLitely, Kayexalate, Lactulose), corticosteroids, insulin

    Medications contributing to hyperkalemia:
    Potassium supplements (K-Dur), potassium salt substitutes, ACE inhibitors, Aldactone, Augmentin, "old" blood transfusions

    Potassium:
    A. The hormone insulin facilitates movement of K+ into cells.
    B. Metabolic acidosis facilitates movement of K+ out of cells (metabolic acidosis = hyperkalemia; metabolic alkalosis = hypokalemia).
    C. Severe exercise and cell trauma (including burns or excessive GI activity) move K+ into blood (out of cells), hyperkalemia.
    D. Aldosterone increases tubular secretion of K+ into urine and thereby decreases serum potassium (This is why the potassium-sparing diruetic aldosterone, which is an aldosterone antagonist, can produce hyperkalemia).
    E. Addison's disease has deficient production of aldosterone. The patient with Addison's is more likely to develop hyperkalemia.
    F. Sammy has lost much fluid during his prolonged diarrhea. He is at risk for hypokalemia.
    G. Cushing's syndrome decreases serum potassium (chronic steroid use will also decrease serum potassium, causing hypokalemia).
    H. Loop diuretics (furosemide) cause serum potassium loss (hypokalemia).

    What precautions are imperative in administration of IV fluids containing potassium?
    Urinary output must be at least 30 ml/hr, IV site must be patent, proper dilution in IV fluid (20 mEq/250ml for peripheral IV site), no more than 20 mEq/hr, must be run on a pump, double check serum lab values, NEVER IV push!

    S/S Hypokalemia:
    Lethargy, leg cramps, muscle weakness, shallow respirations, irregular heart rate (dysrhythmias), hypoactive bowel sounds, nausea and vomiting, flat T waves on ECG

    S/S Hyperkalemia:
    Cardiac (most important): peaked T wave, bradycardia, cardiac arrest
    Mild hyperkalemia: hyperreflexia, muscle twitches
    Severe hyperkalemia: numbness, weakness, paralysis
    GI: increased peristalsis, abdominal cramping with diarrhea, vomiting
    Oliguria

    S/S Hypocalcemia:
    Tetany, positive Chvostek's and Trousseau's signs, paresthesias (tingling of lips and extremities), hyperreflexia, seizures, bleeding, increased peristalsis (diarrhea)

    S/S Hypercalcemia (think malignancy, hyperparathyroidism, prolonged immobility)
    Bone pain, fractures, kidney stones, polyuria, dehydration, blood clots, decreased peristalsis (constipation), hyporeflexia, confusion, lethargy, coma

    Hypocalcemia = bleeding, hypercalcemia = blood clots

    The effect of calcitonin is to lower serum calcium.
    The effect of PTH is to raise serum calcium.
    The effect of vitamin D is to raise serum calcium.
    The effect of PTH is to lower serum phosphate.
    The effect of vitamin D is to raise serum phosphate.

    Hyperphosphatemia or hypophosphatemia.
    A. Chronic use of antacids with aluminum or calcium that bind phosphate: hypophosphatemia
    B. Alcoholism (with associated malnutrition): hypophosphatemia
    C. Phosphate-containing enemas: hyperphosphatemia
    D. Massive trauma: hyperphosphatemia
    E. Renal failure: hyperphosphatemia
    Attached Files
  5. by   RNin2007
    Thank you SO much :bowingpur Vicki!!....you never fail to wow me. Your students are lucky to have you. I am printing these off, and I know I will have this stuff down by Monday for sure =). This is great info, and another angle to look at it compared to my own notes.

    4 more finals, 3 more school days!

    ~J
  6. by   VickyRN
    Quote from RNin2007
    Thank you SO much :bowingpur Vicki!!....you never fail to wow me. Your students are lucky to have you. I am printing these off, and I know I will have this stuff down by Monday for sure =). This is great info, and another angle to look at it compared to my own notes.

    4 more finals, 3 more school days!

    ~J
    Glad to be of assistance and sending warm thoughts your way for great success on your finals. I have also attached the answers to the study guide for your convenience
    Attached Files
  7. by   RNin2007
    I was just sitting here answering some of these thinking to myself, "it sure would be nice to have an answer key..." lol =) I didn't want to push it and ask though....but again, THANKS! I am starting to get a much better understanding of this now.

    I appreciate the well-wishes on my finals for sure! From what I understand Patho/Pharm are the two toughest courses...so hopefully things will be a *little* easier after this term.

    Thanks Vicki,

    ~J

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