2. Electrolytes

3. ELECTROLYTE REGULATION: Cations **  SODIUM Salt intake, Aldosterone, Kidneys  POTASSIUM Kidneys  CALCIUM Parathyroid hormone  MAGNESIUM Kidney Electrolyte Regulation: Anions CHLORIDE Kidneys BICARBONATE Kidneys PHOSPHATE Parathyroid Hormone, Kidneys, Activated Vitamin D

4. ELECTROLYTES: Memorize!!  SODIUM Hyponatremia < 135 mEq/L Hypernatremia > 145 mEq/L  POTASSIUM Hypokalemia < 3.5 mEq/L Hyperkalemia > 5.0 mEq/L  Calcium Hypocalcemia < 8.5 mg/dl Hypercalcemia > 10.0 mg/dl

5. HYPONATREMIA (Na < 135mEq/L)  Overview controls water distribution (principle regulator of extracellular fluid volume) necessary for nerve impulse transmission alterations think “mental/neurological”  Etiology loss of sodium: GI losses, diuretics, adrenal insufficiency, sweating, or gain of water: edematous conditions, excessive hypotonic fluids, SIADH (syndrome inappropriate anti-diuretic hormone – covered in ENDO unit)

6. HYPONATREMIA (cont.)  Physical Assessment/Clinical Manifestations (may include manifestations of dehydration) **altered mental status (increased water content in brain cells!!) headache, depression, personality changes, confusion, lethargy, tremors leading to convulsions & coma nausea, abd. cramps due to hyperactive bowels, diarrhea muscle weakness, diminished deep tendon reflexes  Laboratory = Na< 135 mEq/L

7. Hyponatremia (cont.)  Drug Therapy: Isotonic IV Fluids 0.9% NaCl, Ringer’s Lactate or  3% NaCl only with extreme caution  Diet Therapy Provide Sodium Containing Foods; Restrict Water  NURSING CARE Assess I&O, Weights, Monitor Fluid/GI Losses Monitor for Mental Changes; Safety

8. Where’s the Salt???? Refer to Table 11-6 review sources  Obvious sodium (you can see it)  Sodium as a flavor enhancer  Sodium as a preservative

9. HYPERNATREMIA (Na > 145 mEq/L  Overview Basic problem = Inability to respond to thirst Who is AT RISK?  Young, old, or cognitively impaired  Etiology (UNABLE TO RESPOND TO THIRST) Administration of hypertonic parenteral solutions or tube feedings Excessive intake of sodium either orally or through parenteral or enteral feedings Excessive Intake of Sodium (very excessive!)

10. Hypernatremia  Physical Assessment/Clinical Manifestations Dehydrated brain cells! Neurological/mental changes Altered cerebral function (agitated, irritable, restless, unable to concentrate) progressing to convulsions & coma Thirst, (may have swollen dry tongue & sticky mucous membranes), weight gain Skeletal muscle weakness  Laboratory = Na > 145 mEq/L  Drug Therapy Hypotonic IV Solutions (0.45% NaCl) Water Replacement  NURSING CARE Monitor Fluid Gains & Losses, restrict sodium, give water Monitor Changes in Behavior Institute Safety Precautions ***Provide tap water to tube fed clients***

12. HYPOKALEMIA  Overview Influences skeletal and CARDIAC activity Normal renal function is essential for balance  Interesting facts: Potassium is the primary ICF cation so movement may cause trouble & The kidneys regulate potassium & have trouble holding onto it with some diuretics Fluid loss from the body usually includes potassium since the body conserves it poorly

13. Hypokalemia (remember need on a daily basis) K < 3.5 mEq/L  Etiology: Actual Deficit Excessive loss due to:  Diuretic use (think Loop Diuretics) (also other meds) Especially with digitalis (will discuss in cardiovascular class)  GI losses from diarrhea, vomiting, wound drainage, N/G suction  Heat-induced excessive diaphoresis Inadequate potassium intake:  Prolonged NPO status  Anorexia/starvation  Etiology: Relative deficit  Alkalosis with potassium shift into cells  Hyperinsulinism, total parenteral nutrition (TPN)  IV therapy without potassium

14. HYPOKALEMIA: K < 3.5 mEq/L  Physical Assessment/ Clinical Manifestations CARDIAC DYSRHYTHMIAS (heart beat irregular in a bad way)  Watch Digitalis (digoxin), hypokalemia potentiates toxicity Generalized muscle weakness progressing to paralysis Leg cramps, nausea & vomiting, paresthesias Decreased bowel sounds (paralytic ileus?) Decreased reflexes (hypo-reflexia)  Laboratory = K < 3.5 mEq/L

15. HYPOKALEMIA  Diet Therapy Food sources daily  What is used in place of table salt (NaCl)? Why do we recommend orange juice or bananas? Know food sources of potassium (Table 11-7, p. 153)  Drug Therapy Oral supplementation (caution can overdose)  Know nursing implications for drugs such as K Dur IV (never IV push, always mix & give with care, check kidney function)

16. HYPERKALEMIA (> 5.0 mEq/L)  Etiology Excessive Potassium Intake  Over-ingestion of food/medication  Rapid infusion of IV containing potassium/bolus by mistake Decreased Potassium Excretion  RENAL FAILURE/RENAL DISEASE  Potassium sparing diuretics  Adrenal insufficiency (more on that later)  Etiology Relative Potassium Excess (movement of K+ from intracellular to extracellular space – temporary)  Metabolic acidosis (Exchanges with H+) (Diabetic ketoacidosis – more later)  Marked tissue injuries (K+ released from cells) KCL

17. HYPERKALEMIA (> 5.0 mEq/L)  Physical Assessment/Clinical Manifestations CARDIAC DYSRHYTHMIAS (heart can stop) Heightened neuromuscular activity, diarrhea, intestinal colic, anxiety, paresthesias, irritability, muscle tremors & twitching Later: muscle weakness progressing to paralysis  Laboratory = K > 5.0 mEq/L  HYPERKALEMIA: Drug Therapy Eliminate potassium administration by d/c IV with K+, withhold oral K+, and avoid in diet. Increase potassium excretion by diuretics such as Lasix, or use Kayexalate with Sorbitol (GI excretion of K+, especially for clients with renal failure) Promote the movement of potassium back into the ICF by giving Insulin or Hypertonic Dextrose & Sodium Bicarbonate (emergency measure

18. HYPOCALCEMIA < 8.5 mg/dl)  Overview Most of total body calcium (99%) is found in bones & teeth BUT not measured in blood calcium The remaining 1% is ionized & is measured in blood calcium So Osteoporosis is NOT Hypocalcemia  Osteoporosis is “brittle bones” & occurs after inadequate calcium intake <age 30 or “runs in families”  Symptoms related to skeletal & muscle contraction  Etiology Decreased parathyroid hormone Malabsorption of calcium (Pancreatitis, GI diseases) Marked deficiencies of dietary calcium and/or Vit D  Laboratory = Ca < 8.5 mg/dl

19. HYPOCALCEMIA: Physical Assessment/ Clinical Manifestations = TETANY, paresthesias Bronchial muscle spasm, laryngospasm leading to respiratory arrest

20. Hypocalcemia: Calcium Food Sources (which 2 do not belong? broccoli cheese Cream cheese Ice cream Spinach Sardines yogurt Canned salmon tofu Skim milk

21. HYPOCALCEMIA <8.5 mg/dl  Diet Therapy Food sources of Calcium (Table 11-8, p. 153) **know for exam Supplementation  Drug Therapy Oral calcium IV Calcium (with caution) Vitamin D  Interventions Protect from injury

22. HYPERCALCEMIA >10.0 mg  Etiology Overuse of calcium supplements/antacids/Vit D MALIGNANCY (why??) Altered GI metabolism Hyperparathyroidism  Physical Assessment/Clinical Manifestations Decreased peristalsis resulting on constipation Profound MUSCLE WEAKNESS, FLACCIDITY Cardiac dysrhythmias  Drug Therapy Administer IV 0.9% NaCl (hemodilution) Diuretics (excrete calcium & sodium) Calcitonin & other calcium binding drugs  Interventions Dialysis Cardiac Monitoring Protect from injury Avoid constipation