3.2 Electrolyte Balance Flashcards
Physiological Factors Affecting Electrolyte Balance
- Kidneys excrete 1 electrolyte in replacement of another for example na/k or ca/p
- Electric neutrality is a must between body compartments. Even a small difference in mEq difference is enough to be a voltage difference.
Sodium/Chloride Balance
*Sodium (na+) 135-145 mEq/L
Sodium (Think Brain)
- Na+ consists of 90% of ECF Cations
- Regulates osmotic forces and water balance.
- Balance is maintained by kidneys and hormonal mediators.
- Sodium also regulates osmolarity, neuromuscular function for conduction of impulses, regulation of acid base balance in conjunction with HCO3, and membrane transport
Sodium/Chloride Balance
Chloride (Cl-) 95 - 105 mEq/L
- Major anion in the ECF.
- Provides electroneutrality
- Undergoes passive transport and follows active transport of sodium.
- Concentration of chloride varies inversely with concentration of bicarbonate (HCO3-)
Hyponatremia (Low Sodium)
3 Categories
- Sodium Loss, Water Gain, Insufficient Sodium Intake
Etiologies
Vomiting, Diarrhea, Fistulas, Nasogastric Suctioning (NG), Wound Drainage, Excessive Sweating, Burns, Salt Losing, Diuretics, SIADH, Adrenal Insufficiency.
Pathophysiology
- Hypoosmolar fluid shifts from ECF to ICF resulting in cellular swelling and potential for abnormal cell depolarization/repolarization.
Hyponatremia (cont)
Clinical Manifestations
Depressed Reflexes, Muscle Cramps, Lethargy, Confusion, Seizure, Coma
Potential Complications
Severe neurological changes. Assess neuro signs and GI Symptoms, maintain seizure precaution and strict fluid restrictions.
Management
- If caused by water excess then fluid restriction
- If caused by abnormal fluid loss then fluid replacement containing sodium. (0.9% Sodium Chloride Solution)
- Severe deficit and symptoms like seizures give small amounts of IV hypertonic saline solution (3% NaCl)
Hypernatremia (Excess Salt)
Etiology (causes)
- Acute Gain (Inappropriate administration of hypertonic saline solution or over secretion of aldosterone)
- Net Loss of water (fever, respiratory infection, profuse sweating, diarrhea, polyuria, diabetes)
Pathophysiology
- Hypertonicity of ECF and results in cellular dehydration
Clinical Manifestation
Thirst, Dry Mucous Membranes, Muscle Twitching, Hyperreflexia, Pulmonary Edema, Headaches and Seizures.
Hypernatremia (cont)
Potential Complications
- Seizure, Coma leading to irreversible brain damage
Nursing Management
- Maintain fluid balance. Return sodium to normal and prevent injury. Replace fluid deficit, monitor intake and output (I&O), daily weights, vital signs, assess skin turgor.
Adjustments to sodium should be slow and steady.
Decrease patient risk of injury by monitoring neuro signs, repositioning, and other safety measures.
Potassium (K+)
Potassium
3.5 - 5 mEq/L (ECF)
140 - 150 mEq/L (ICF)
(Think Heart)
- Major Intracellular Cation
- Major determinant of resting membrane potential for nerve impulse, cardiac rhythm, and muscle contraction
- Potassium is exchanged for (H+) in blood in acid base buffering system.
- Acidosis - Too much H+ in ECF so Potassium leaves cells and H+ goes into cells. This causes Hyperkalemia.
- Alkalosis - Potassium goes into cells and hydrogen leaves cells. This causes Hypokalemia.
Potassium (cont)
- Intracellular concentration is maintained by sodium-potassium pump in cells. Potassium moves out of cells when channels are open. Extracellular concentration is regulated by kidneys. Potassium is filtered in glomerulus and ~90% is reabsorbed in proximal tubule.
Hormonal Influence of Potassium
Aldosterone - Stimulated by increase in K+. Increased levels are then excreted by kidneys and sweat glands.
Catecholamines (epinephrine) - Influences movement of K+ into cells.
Insulin - Influences movement of K+ into cells.
Hypokalemia (Low Potassium)
Common Causes
- Deficit in potassium stores or abnormal movement of potassium into cells.
- Excess loss from kidneys/GI Tract
- Renal disorders, vomiting, diarrhea, intestinal drainage tubes, laxative abuse, diuretics.
Clinical Manifestations
- Cardiac Dysrhythmia, weak irregular pulse, weakness, confusion, muscle cramp, paralysis.
Potential complications
- Dysrhythmias
Hypokalemia (cont)
Management
- Oral or IV Potassium supplements.
- IV MUST BE DILUTED (do not exceed 10-20 mEq/hour)
to prevent hyperkalemia and cardiac arrest.
Hyperkalemia (Excess Potassium)
- Clinically significant at 6.0 mEq/L
- Life threatening at 8.0 mEq/L
80% of potassium leaves body from kidneys.
Etiology
- Decreased renal elimination, increased intake, burns, extensive surgery, trauma, crushing injuries, insulin deficits, decreased secretion of aldosterone,
Clinical Manifestations
- Dysrhythmia, cardiac arrest, muscle weakness, paresthesia, flaccid paralysis.
Hyperkalemia (cont)
Potential Complications
Dysrhythmia
Management
- Eliminate oral and parental Potassium intake.
- Increase elimination of K+ with diuretics, dialysis, kayexalate (K+ binding agent), force potassium into ICF with Sodium Bicarbonate (Base). Administer Calcium Gluconate IV to protect heart from elevated potassium.
Calcium (Ca+)
- 5 - 10.5 mg/dL
- Second Major ECF Cation
- More than 99% is combined with phosphorous and concentrated in skeletal system.
- 50% of calcium in the blood is bound to proteins (albumin)
- Calcium increased in Alkalemia and decreased in acidemia. (Inverse relationship with hydrogen)
What does Calcium Do?
- With phosphate it forms strong bones.
- Blood clotting
- Membrane stability
- Neuromuscular excitability
- Muscle contractibility
- Absorbed in intestines with influence of Vitamin D
- Dietary Ca is excreted in colon and kidneys.
- Reabsorption of calcium in proximal tubule (50-60%)
- Reabsorption of calcium in loop of Henle (30-35%)
What does calcium do (cont)
- Inverse relationship with phosphorous.
- Parathyroid gland regulates ca+ and po4 based on serum levels of ionized ca+.
- Ca+ and PO4 are increased by bone reabsorption.
- Renal reabsorption of Ca+ decreases reabsorption of PO4 and stimulates renal synthesis of Vitamin D
Calcitonin - inhibits reabsorption of osteoclasts when calcium serum levels are elevated - Vitamin D increases GI absorption of CA and PO
Calcium Acid Base Balance
In acidosis - Calcium Increases
In Alkalosis - Calcium Decreases
Hypocalcemia (Less than 8.5 mg/dL)
Etiology - Decreased production of parathyroid hormone. Thyroidectomy, Acute pancreatitis, multiple blood transfusions, alkalosis, decreased intake of calcium or vitamin D, renal failure, drug therapies.
Clinical Manifestation
- Positive Trousseau or Chvostek sign, laryngeal stridor, dysphagia, tetany, tingling around mouth and extremities, hyperactive deep tendon reflexes, seizures.
Chvostek sign - tap cheek and see mouth reflex
Trousseau Sign - Blood pressure cuff +20 mmHg to see wrist hyperflexion
Hypocalcemia (cont)
Management
Calcium supplements or in severe cases IV Calcium Gluconate or Calcium Chloride
(Check medication interactions with calcium)
- Blood pressure beta blockers (atenolol) decrease calcium absorption taken 2 hours of taking calcium)
- Antacids containing aluminum may increase blood levels of aluminum.
- Cholesterol lowering bile acid like colestipol, decrease calcium absorption and increase calcium excretion.
- Estrogen can cause increase in calcium
- High levels of calcium can increase digoxin toxicity.
- Diuretics - Can increase or decrease calcium
- Certain antibiotics can decrease calcium supplements.
Hypercalcemia
Etiology
Hyperparathyroidism, malignancy, vitamin D overdose, prolonged immobilization, decreased renal excretion in renal failure, drug therapy with thiazides
Clinical Manifestations
Decreased Memory, confusion, disorientation, slurred speech, fatigue, lethargy, constipation, anorexia, nausea, vomiting, muscle weakness, incoordination, excessive thirst, hypoactive deep tendon reflex, mental status change.
Hypercalcemia
Potential complications
Dysrhythmia
Management
Parathyroidectomy, cancer therapy, dialysis. Medications like calcitonin, a hormone from salmon controls calcium levels in blood, diuretics may be used to lower calcium quickly, bisphosphates like pamidronate, zoledronate inhibit bone loss.
Hypophosphatemia (Low PO4)
Etiology
Increased Renal Excretion, Intestinal Malabsorption (Vitamin D Deficiency), Magnesium/Aluminum antacids, hyperparathyroidism.
Clinical Manifestations
Muscle Weakness, Fatigue, Dysrhythmia, bone pain, fractures, irritability, confusion, coma
Management
Dietary replacement of phosphorous and phosphate supplementation
Hyperphosphatemia (High PO4)
Etiology
Massive cellular destruction (tumor lysis syndrome), renal failure (CRF), hypoparathyroidism
Clinical Manifestations
Decreased serum calcium, excess phosphate stimulates osteogenic transformation of vascular smooth muscle cells, resulting in accelerated vascular calcification.
Management
Administration of aluminum hydroxide as a phosphate binder especially in CRF. Sever cases dialysis
Magnesium
- 4 - 2.1 mg/dL
- Major intracellular cation. 50-60% in bones, 30% in cells
- Coenzyme in metabolism of protein and carbohydrates and a large number of intracellular enzymatic reactions including protein synthesis. Key in neuromuscular excitability (inhibits muscle excitability)
- Regulated by kidneys. Factors that regulate calcium also influence magnesium balance.
Hypomagnesemia (low magnesium)
Etiology
Inadequate intake, chronic disease, alcohol use disorder, GI losses and renal losses.
Clinical Manifestation
Neuromuscular irritability, tremors, fasciculations, tetany. Chvostek and Trousseau signs, and convulsions. Apathy, depression, and muscle cramps.
Management
Magnesium replacement
Hypermagnesemia (High Magnesium)
Etiology
Increased intake with renal insufficiency, overuse of magnesium antacids, laxatives with magnesium and dehydration.
Clinical Manifestation
Lethargy, drowsiness, nausea, vomiting, impaired reflexes (hypoactive), respiratory and cardiac arrest, hot, flushed skin, hypotension, bradycardia, decreased respiratory rate.
Management
Prevention is key. Fluids to promote urinary excretion.
Emergency treatment of administration of calcium chloride via IV. Possible dialysis.
