ELECTROLYTE
PRESENTED BY- DR. SUJAY S. PATILPART 1 RESIDENT
DEPT. OF OMFS
CATIONSCATIONS ANIONSANIONSNa- 135-145 m Eq/LNa- 135-145 m Eq/LK- 3.5 – 5.0 m Eq/LK- 3.5 – 5.0 m Eq/LCa- 4.5-5.5 mEq/LCa- 4.5-5.5 mEq/LMg -1.5 – 2.5 mEq/LMg -1.5 – 2.5 mEq/L
HCO3- 22-26 mEq/LHCO3- 22-26 mEq/LCl- 96-106 mEq/LCl- 96-106 mEq/LPO4 – 1.2 -3.0 mEq/LPO4 – 1.2 -3.0 mEq/L
Electrolytes – – These are chemical substances which when dissolved, dissociate into ions and pass electrical potential..
SODIUM
HYPONATREMIA (<135MEQ/L)
Contributing FactorsExcessive diaphoresisWound DrainageNPOCHFLow salt dietRenal DiseaseDiuretics
HYPONATREMIA (<135MEQ/L)
Assessment findings: Neuro - Generalized skeletal muscle weakness. Headache / personality changes.
Resp.- Shallow respirationsCV - Cardiac changes depend on fluid volumeGI – Increased GI motility, Nausea, Diarrhea (explosive)GU - Increased urine output
HYPONATREMIA (<135MEQ/L)
Interventions/TreatmentRestore Na levels to normal and prevent further decreases in Na.Drug Therapy – (FVD) - IV therapy to restore both fluid and Na. If severe may see 2-3% saline.
(FVE) – Administer osmotic diuretic (Mannitol) to excrete the water rather than the sodium.
Increase oral sodium intake and restrict oral fluid intake.
HYPERNATREMIA (>145MEQ/L)
Contributing FactorsHyperaldosteronismRenal failureCorticosteroidsIncrease in oral Na intakeNa containing IV fluidsDecreased urine output with increased urine concentration
HYPERNATREMIA (>145MEQ/L)
Contributing factors (cont’d):DiarrheaDehydrationFeverHyperventilation
HYPERNATREMIA (>145MEQ/L) Assessment findings: Neuro - Spontaneous muscle twitches. Irregular contractions. Skeletal muscle weakness. Diminished deep tendon reflexes
Resp. – Pulmonary edemaCV – Diminished CO. HR and BP depend on vascular volume.
HYPERNATREMIA (>145MEQ/L)
GU – Dec. urine output. Inc. specific gravity
Skin – Dry, flaky skin. Edema r/t fluid volume changes.
HYPERNATREMIA (>145MEQ/L)
Interventions/TreatmentDrug therapy (FVD) .45% NSS. If caused by both Na and fluid loss, will administer NaCL. If inadequate renal excretion of sodium, will administer diuretics.
Diet therapyMild – Ensure water intake
POTASSIUM
Low concentrations in ECF
Normal 3.5-5.0 mEq/L
Major ICF cation
Normal daily intake : 40 -60 mEq/L
The rate of potassium excretion is regulated by aldosterone; aldosterone stimulates potassium ion excretion.
HYPOKALEMIA (<3.5MEQ/L)
Pathophysiology – Decrease in K+ causes decreased excitability of cells, therefore cells are less responsive to normal stimuli
HYPOKALEMIA (<3.5MEQ/L)
Contributing factors:DiureticsShift into cellsDigitalisWater intoxicationCorticosteroidsDiarrheaVomiting
HYPOKALEMIA (<3.5MEQ/L)
InterventionsAssess and identify those at riskEncourage potassium-rich foodsK+ replacement (IV or PO)Monitor lab valuesD/c potassium-wasting diureticsTreat underlying cause
HYPERKALEMIA (>5.0MEQ/L)
Pathophysiology – An inc. in K+ causes increased excitability of cells.
HYPERKALEMIA (>5.0MEQ/L)
Contributing factors:Increase in K+ intakeRenal failureK+ sparing diureticsShift of K+ out of the cells
HYPERKALEMIA (>5.0MEQ/L)
InterventionsNeed to restore normal K+ balance:Eliminate K+ administrationInc. K+ excretionLasixKayexalate (Polystyrene sulfonate)
Infuse glucose and insulinCardiac Monitoring
CHLORIDE Chloride (Cl-) - 95-103 mEq/liter
Major ECF anionhelps balance osmotic potential and electrostatic equilibrium between fluid compartments
plasma membranes tend to be leaky to Cl- anions
Regulation:aldosterone
HOMEOSTATIC IMBALANCES
Hypochloremia - results in muscle spasms, coma [usually occurs with hyponatremia] often due to prolonged vomiting
Causes:
metabolic alkalosis
Respiratory acidosis
emphysema
Adrenal cortical insufficiency
thiazides
diarrhea
HYPERCHLOREMIA
Causes: hyper chloremic acidosis
Respiratory alkalosisDehydrationDiabetes insipidus renal tubular acidosis
CALCIUM
Normal 4.5-5.5 mEq/L
99% of Ca in bones, other 1% in ECF and soft tissues
Total Calcium – bound to protein – levels influenced by nutritional state
Ionized Calcium – used in physiologic activities – crucial for neuromuscular activity
CALCIUM
Required for blood coagulation, neuromuscular contraction, enzymatic activity, and strength and durability of bones and teeth
Nerve cell membranes less excitable with enough calcium
Ca absorption and concentration influenced by Vit D, calcitriol (active form of Vitamin D), PTH, calcitonin, serum concentration of Ca and Ph.
HYPOCALCEMIA (<9.0MG/DL)
Contributing factors:Dec. oral intakeLactose intoleranceDec. Vitamin D intakeEnd stage renal diseaseDiarrhea
HYPOCALCEMIA (<9.0MG/DL)
Contributing factors (cont’d):
Acute pancreatitis
Hyperphosphatemia
Immobility
Removal or destruction of parathyroid gland
HYPOCALCEMIA (<9.0MG/DL) Assessment findings: Neuro –Irritable muscle twitches.Positive Trousseau’s sign. Positive Chvostek’s sign.
Resp. – Resp. failure d/t muscle tetany.CV – Dec. HR., dec. BP, diminished peripheral pulsesGI – Inc. motility. Inc. BS. Diarrhea
HYPOCALCEMIA (<9.0MG/DL)
Interventions/TreatmentDrug TherapyCalcium supplementsVitamin D
Diet TherapyHigh calcium diet
Prevention of InjurySeizure precautions
HYPERCALCEMIA (>10.5MG/DL)
Contributing factors:Excessive calcium intakeExcessive vitamin D intakeRenal failureHyperparathyroidismMalignancyHyperthyroidism
HYPERCALCEMIA (>10.5MG/DL)
Assessment findings: Neuro – Disorientation, lethargy, coma, profound muscle weakness Resp. – Ineffective resp. movement CV - Inc. HR, Inc. BP. , Bounding peripheral pulses, Positive Homan’s sign. Late Phase – Bradycardia, Cardiac arrest GI – Dec. motility. Dec. BS. Constipation GU – Inc. urine output. Formation of renal calculi
HYPERCALCEMIA (>10.5MG/DL) Interventions/Treatment Eliminate calcium administration Drug Therapy Isotonic NaCL (Inc. the excretion of Ca) Diuretics Calcium reabsorption inhibitors (Phosphorus) Cardiac Monitoring
MAGNESIUM
Normal 1.5 to 2.5 mEq/L
Ensures K and Na transport across cell membrane
Important in CHO and protein metabolism
Plays significant role in nerve cell conduction
Important in transmitting CNS messages and maintaining neuromuscular activity
HYPOMAGNESEMIA (<1.4MEQ/L) Contributing factors: Malnutrition Starvation Diuretics Aminoglcoside antibiotics Hyperglycemia Insulin administration
HYPOMAGNESEMIA (<1.4MEQ/L)
Assessment findings:*Neuro - Positive Trousseau’s sign. Positive Chvostek’s sign. Hyperreflexia. Seizures*CV – ECG changes. Dysrhythmias. HTN*Resp. – Shallow resp.*GI – Dec. motility. Anorexia. Nausea
HYPOMAGNESEMIA (<1.4MEQ/L) Interventions: Eliminate contributing drugs IV MgSO4 Assess DTR’s hourly with MgSO4 Diet Therapy
HYPERMAGNESEMIA (>2.0MEQ/L) Contributing factors: Increased Mag intake Decreased renal excretion
HYPERMAGNESEMIA (>2.0MEQ/L) Assessment findings:Neuro – Reduced or weak DTR’s. Weak voluntary muscle contractions. Drowsy to the point of lethargyCV – Bradycardia, peripheral vasodilatation, hypotension. ECG changes.
HYPERMAGNESEMIA (>2.0MG/DL) Interventions Eliminate contributing drugs Administer diuretic Calcium gluconate reverses cardiac effects Diet restrictions
PHOSPHOROUS Normal 2.5-4.9 mg/dL
Intracellular mineral
Essential to tissue oxygenation, normal CNS function and movement of glucose into cells, assists in regulation of Ca and maintenance of acid-base balance
Influenced by parathyroid hormone and has inverse relationship to Calcium
HYPOPHOSPHATEMIA (<2.5MG/L) Contributing Factors: Malnutrition Starvation Hypercalcemia Renal failure Uncontrolled DM
HYPOPHOSPHATEMIA (<2.5MG/L) Assessment findings: (Chart 13-7)Neuro – Irritability, confusionCV – Dec. contractilityResp. – Shallow respirationsMusculoskeletal - RhabdomyolysisHematologic – Inc. bleeding
Dec. platelet aggregation
HYPOPHOSPHATEMIA (<2.5MG/L) Interventions Treat underlying cause Oral replacement with vit. D IV phosphorus (Severe) Diet therapy
Foods high in oral phosphate
HYPERPHOSPHATEMIA (>4.5MG/L) Causes few direct problems with body function. Care is directed to hypocalcemia. Rarely occurs