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Sodium
• Cation mainly found in the ECF
• Responsible for water retention Hyponatremia: S/SX:
• Normal range: 135 – 145 mEq/L • N/V, diarrhea Clinical Management:
Functions: • Tachycardia, hypotension • Hyponatremia: NS (0.9%) or 3% salt
• NM: transmission and conduction of nerve • Headaches, lethargy, confusion, seizures solution
impulses (Na-K pump) • Muscular weakness • Hypernatremia: diuretics
• Responsible for the osmolality of vascular • Dry skin, pale, dry mm Clinical considerations
fluids Hypernatremia: S/SX: • Sodium causes water retention
• Cellular: Na pump action. Na shifts into • N/V, anorexia • Vomiting causes sodium, chloride losses,
cells as K shifts out, repeatedly, to maintain • Tachycardia, possible hypertension and diarrhea causes sodium, chloride, and
water balance and NM activity. When Na • Restlessness, agitation, stupor bicarbonate losses
shifts into the cell, it stimulates • Muscular twitching, tremor, hyperreflexia • A 3% saline should be given for severe
depolarization (cell activity); and when Na • Flushed, dry skin, dry, sticky membranes serum sodium deficit, check for pulmonary
shifts out of the cell, K shifts back into the Drugs that influence levels: edema
cell, and repolarization occurs • Na and K have opposite effects on cellular
• Hyponatremia: diuretics-sodium excretion
• Na combines readily with Cl or bicarbonate activity.
• Hypernatremia: corticosteroids-promote Na
to regulate the acid-base imbalance • Steroids promote Na retention and thus
retention & K excretion
water retention
Calcium
• Electrolyte found in the ICF Hypocalcemia: causes • Impaired blood clotting • Calcitonin
and ECF • Lack of intake Hypercalcemia: S/SX • IV phosphates
• Normal range: 9 – 11 • Chronic diarrhea • Muscles flabby Clinical Considerations
mg/dL • Renal failure • Cardiac arrest • Administer oral supplements
Functions: • Hypoparathyroidism • Pathologic fractures with vitamin D, give 30 in
• Causes transmission of nerve • Increased phosphorus level • Calcium stones before meals
impulses and contraction of Hypercalcemia: causes • Flank pain • Dilute IV calcium salts in
skeletal muscles, • Thiazide diuretics Hypocalcemia: Mgmt 5% dextrose
myocardium • Malignant bone tumors • Dietary • Infiltration can cause
• Maintenance of cellular • Hyperparathyroidism • Oral supplements sloughing
permeability • Decreased phosphorus level • Vitamin D • Elevated levels can enhance
• Coagulation of blood. teeth, • Prolonged immobilization • IV calcium salts the action of digoxin
bone formation Hypocalcemia: S/SX: Hypercalcemia: Mgmt. • Diuretics (loop) and steroids
• Tetany • IV normal saline can decrease levels
• +Chvostek’s & Trouseau’s • Diuretics • Thiazide increase levels
sign • Loop (furosemide- Lasix)
Acid-Base Balance
• Acids :Produced as end products of metabolism
• Bases : Neutralize & promote excretion of acids
• Health Problems Buffers
• Diabetes Mellitus • Substances that either bind to or release hydrogen ions to prevent drastic
• COPD changes in pH
• Kidney disease Buffer Systems:
Normals: • Bicarbonate-carbonic acid
• pH: 7.35-7.45 • Phosphate buffer system
• PaCo2: 35-45 (carbon dioxide) • Hemoglobin-oxyhemoglobin buffer system
• HCO3: 22-26 (bicarb) • Protein buffer system
Respiratory component: release of CO2 & H2O from body
Renal component: reabsorb & manufacture bicarb to buffer acid, excrete H into urine
Metabolic Acidosis
• ↓ pH, ↓ HCO3, ↓ Anion gap
• Decrease in bicarbonate concentration or acid excess S/S
Causes: •
Increased respiratory rate & depth: Kussmaul respirations
• Lactic acidosis (anaerobic metabolism) • HA, lethargy leads to coma
• Ketoacidosis • N&V, diarrhea, abdominal pain
• Ingestion of acidic substances • Elevated serum K+ (shift of K+ out of cell, H+ into cell)
• renal disease Loss of bicarbonate or reduced H+ excretion Compensation:
• ↑ RR to blow off CO2 (↓acid)
Metabolic Alkalosis
• ↑ pH, ↑ HCO3 • Hyperaldosterone (steroids) loss of chloride retention of bicarb
• Increase in bicarbonate concentration or loss of the hydrogen ion in the ECF S/S:
Causes: • Weakness, muscle cramps, hyperactive reflexes, dysrythmia (hypokalemia)
• Vomiting, NG drainage (loss of acid) • Decreased respiratory depth and rate (leads to elevated pCo2 levels)
• Diuretics loss of chloride retention of bicarb • Confusion, seizure
• Excessive ingestion of antacids or IV bicarb Compensation:
• ↓ RR to retain CO2 (retain acid)
Respiratory Acidosis
• An increase in carbonic acid / retention of carbon dioxide (pCo2) • Pulmonary embolism, pulmonary edema
• ↓ pH, ↑ Pco2 S/S
Causes: • SOB, restlessness
• Respiratory depression, drugs, head injury • Lethargy, disorientation, seizure, coma
• Respiratory muscle paralysis • Warm flushed skin (vasodilation from increased CO2 levels)
• Disorders of the lung tissue (COPD, pneumonia) Compensation:
• Kidneys ↑ H excretion & bicarb reabsorption
Respiratory Alkalosis
• Excessive respiratory rate and depth, reduction in carbon dioxide levels S/S
• ↑ pH, ↓ Pco2 • Dizziness confusion ( cerebral vasoconstriction)
Causes: • Paresthesias, carpopedal spasm, (hypocalcemia)
• Hyperventilation (hysteria, mechanical ventilation) • Rapid deep respirations
• Hypoxemia in pulmonary disease or CHF Compensation:
• Hypermetabolic states (fever, anemia, thyroid storm) • Kidneys ↓ H excretion, ↑ bicarb reabsorption