Dehydration and Fluid Balance Quiz

Homeostasis is the state of equilibrium in the body, naturally maintained by adaptive responses. Body fluids and electrolytes are constantly maintained within narrow limits.
Fluid and Electrolyte Imbalances can be directly caused by illness or disease (e.g., burns, heart failure), or as a result of therapeutic measures (e.g., IV fluids, diuretics).
Water status affects red blood cells (RBCs). In hypotonic solutions, water moves into the cell, causing it to swell. In isotonic solutions, there's no net movement of water. In hypertonic solutions, water moves out of the cell, causing it to shrink.
Gerontologic considerations for fluid and electrolytes include structural changes in the kidneys decreasing glomerular filtration rate (GFR) and renal blood flow, leading to impaired electrolyte balance. Decreased subcutaneous tissue and reduced thirst response increase the risk of dehydration.
Extracellular Fluid (ECF) volume imbalances include deficits (hypovolemia, abnormal loss of body fluids, inadequate fluid intake, shift of plasma to interstitial fluid) and excesses (hypervolemia, excessive fluid intake, or abnormal fluid retention).
Nursing interventions include monitoring vital signs (such as heart rate, blood pressure, respiratory rate, oxygen saturation), input and output, specific gravity, orthostatic vital signs, neurologic status, lab work, daily weights, and skin assessment.

Hypernatremia (>145 mEq/L) can result from excessive sodium intake (IV fluids, tube feedings without water, near-drowning in salt water) or inadequate water intake (unconscious or cognitively impaired persons).
Excessive water loss (e.g., high fever, heat stroke, osmotic diuretic therapy, diarrhea) can also lead to hypernatremia.
Diseases like diabetes insipidus, hyperaldosteronism, and Cushing's syndrome may contribute to hypernatremia.
Expected findings in hypernatremia include a decreased extracellular fluid volume, postural hypotension, tachycardia, decreased intravascular volume, elevated temperature, restlessness, agitation, lethargy, seizures, coma, weakness, muscle cramps, intense thirst, and flushed skin.
Treatment for water deficit involves preventing further water loss, providing free water replacement, and administering hypotonic solutions (e.g., D5W + 0.45% NS) if PO isn't tolerated. Treatment for excess sodium intake involves diuretics to promote sodium excretion and sodium-restricted diets.

Potassium levels should be between 3.5-5.0 mEq/L. Potassium comes from fruits, vegetables (potatoes, bananas, leafy greens), salt substitutes, potassium medications (PO, IV), and stored blood.
Hyperkalemia (>5.0 mEq/L) can result from excess intake (parenteral intake, potassium-containing medications, potassium substitutes) or failure to eliminate potassium (kidney disease, adrenal insufficiency, medications (ACE inhibitors, ARBs, NSAIDs, potassium-sparing diuretics), and massive cell injury (trauma, sepsis, tumor lysis syndrome).
Expected findings with hyperkalemia include slow irregular heart rate, hypotension, restlessness, irritability, weakness, ascending paralysis, paresthesias, PVCs, ventricular fibrillation, peaked T waves, wide QRS complexes, increased motility, hyperactive bowel sounds, diarrhea, and oliguria.
Treatment for hyperkalemia involves stopping potassium intake, promoting potassium excretion (loop diuretics, sodium polystyrene sulfonate, calcium gluconate), and dialysis if needed.

Hypokalemia (<3.5 mEq/L) can result from GI losses (diarrhea, vomiting, NG suction), renal losses (diuretics), diaphoresis, or dialysis, increased insulin release, insulin therapy, alkalosis, increased epinephrine, or lack of potassium intake (crash diets, diet low in potassium, prolonged NPO status, malabsorption).
Expected findings with hypokalemia include a slow irregular heart rate, hypotension, anxiety, lethargy, mental status changes that may progress to coma, weakness, decreased deep tendon reflexes, flattened T waves, ST depression, prolonged PR interval, hypoactive bowel sounds, vomiting, cramping, abdominal distention, and shallow breathing.
Treatment for hypokalemia involves increasing potassium intake (oral supplements, potassium chloride tablets or elixir) and administering IV potassium chloride cautiously, over a period of at least one hour, with close cardiac monitoring, if needed.

Calcium levels range from 9.0-10.5 mg/dL. Calcium comes from ingested foods, and requires vitamin D for absorption. Primarily found in bones and teeth, calcium levels are affected by changes in pH and albumin levels.
Hypercalcemia (>10.5 mg/dL) may arise from hyperparathyroidism (2/3 of cases), immobilization, excessive calcium intake, or thiazide diuretics. Paget's disease, adrenal insufficiency, mycobacterium infection, or cancer (hematological or bone mets) are additional causes.
Expected findings with hypercalcemia include increased blood pressure, lethargy, weakness, fatigue, decreased memory, confusion, psychosis , decreased deep tendon reflexes, bone pain and fractures, shortened ST segment, shortened QT interval, ventricular dysrhythmias, anorexia, nausea, vomiting, polyuria, dehydration,renal calculi, and kidney stones.
Nursing interventions include restricting calcium intake, promoting calcium excretion (hydration), encouraging mobilization, and managing severe cases with synthetic calcitonin or bisphosphonates.

Hypocalcemia (<9.0 mg/dL) may occur due to hypoparathyroidism, renal insufficiency, acute pancreatitis, high phosphate levels, vitamin D deficiency, low magnesium levels, diuretics, diarrhea or laxative abuse, or chronic alcohol use.
Expected findings with hypocalcemia include decreased blood pressure, weakness, fatigue, confusion, depression, hyperreflexia, muscle cramps, numbness or tingling, Chvostek's sign, Trousseau's sign, elongated ST segment, prolonged QT interval, ventricular tachycardia, hyperactive bowel sounds, diarrhea,and abdominal cramps.
Treatment for hypocalcemia involves treating the underlying cause, providing calcium and vitamin D supplements orally or intravenously depending on severity, and controlling symptoms like muscle spasms using CO2 retention techniques.

Magnesium levels range from 1.5-2.5 mEq/L.
Hypermagnesemia (>2.5 mEq/L) can arise from renal failure, excessive magnesium administration (e.g., eclampsia).
Expected findings with hypermagnesemia include lethargy, drowsiness, central nervous system (CNS) depression, decreased deep tendon reflexes, muscle weakness, warm flushed skin, and hypothermia, nausea, vomiting, and heart block.
Treatment for hypermagnesemia includes preventing further magnesium intake, administering calcium gluconate or calcium chloride (IV) or fluids and diuretics (IV Lasix) to promote excretion, and dialysis if needed.
Hypomagnesemia (<1.5 mEq/L) can result from malabsorption, alcoholism, malnutrition, diuretics,or hyperaldosteronism
Expected findings with hypomagnesemia include confusion, seizures, hyperreflexia, muscle cramps, and dysrhythmia.
Treatment for hypomagnesemia involves treating the underlying condition, providing oral magnesium supplements, and in severe cases, administering intravenous or intramuscular magnesium.