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ELECTROLYTE
PRESENTED BY- DR. SUJAY S. PATIL
PART 1 RESIDENT
DEPT. OF OMFS
CATIONSCATIONS ANIONSANIONS
Na- 135-145 m Eq/LNa- 135-145 m Eq/L
K- 3.5 – 5.0 m Eq/LK- 3.5 – 5.0 m Eq/L
Ca- 4.5-5.5 mEq/LCa- 4.5-5.5 mEq/L
Mg -1.5 – 2.5 mEq/LMg -1.5 – 2.5 mEq/L
HCO3- 22-26 mEq/LHCO3- 22-26 mEq/L
Cl- 96-106 mEq/LCl- 96-106 mEq/L
PO4 – 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 Factors
Excessive diaphoresis
Wound Drainage
NPO
CHF
Low salt diet
Renal Disease
Diuretics
HYPONATREMIA (<135MEQ/L)
Assessment findings:
Neuro - Generalized skeletal muscle weakness. Headache /
personality changes.
Resp.- Shallow respirations
CV - Cardiac changes depend on fluid volume
GI – Increased GI motility, Nausea, Diarrhea (explosive)
GU - Increased urine output
HYPONATREMIA (<135MEQ/L)
Interventions/Treatment
Restore 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 Factors
Hyperaldosteronism
Renal failure
Corticosteroids
Increase in oral Na intake
Na containing IV fluids
Decreased urine output with increased urine concentration
HYPERNATREMIA (>145MEQ/L)
Contributing factors (cont’d):
Diarrhea
Dehydration
Fever
Hyperventilation
HYPERNATREMIA (>145MEQ/L)
Assessment findings:
Neuro - Spontaneous muscle twitches. Irregular contractions.
Skeletal muscle weakness. Diminished deep tendon reflexes
Resp. – Pulmonary edema
CV – 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/Treatment
Drug 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 therapy
Mild – 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:
Diuretics
Shift into cells
Digitalis
Water intoxication
Corticosteroids
Diarrhea
Vomiting
HYPOKALEMIA (<3.5MEQ/L)
Interventions
Assess and identify those at risk
Encourage potassium-rich foods
K+ replacement (IV or PO)
Monitor lab values
D/c potassium-wasting diuretics
Treat 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+ intake
Renal failure
K+ sparing diuretics
Shift of K+ out of the cells
HYPERKALEMIA (>5.0MEQ/L)
Interventions
Need to restore normal K+ balance:
Eliminate K+ administration
Inc. K+ excretion
Lasix
Kayexalate (Polystyrene sulfonate)
Infuse glucose and insulin
Cardiac Monitoring
CHLORIDE
Chloride (Cl-
) - 95-103 mEq/liter
Major ECF anion
helps 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 alkalosis
Dehydration
Diabetes 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 intake
Lactose intolerance
Dec. Vitamin D intake
End stage renal disease
Diarrhea
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 pulses
GI – Inc. motility. Inc. BS. Diarrhea
HYPOCALCEMIA (<9.0MG/DL)
Interventions/Treatment
Drug Therapy
Calcium supplements
Vitamin D
Diet Therapy
High calcium diet
Prevention of Injury
Seizure precautions
HYPERCALCEMIA (>10.5MG/DL)
Contributing factors:
Excessive calcium intake
Excessive vitamin D intake
Renal failure
Hyperparathyroidism
Malignancy
Hyperthyroidism
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 lethargy
CV – 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, confusion
CV – Dec. contractility
Resp. – Shallow respirations
Musculoskeletal - Rhabdomyolysis
Hematologic – 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

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Administration of Electrolytes in traumatic injuries

Editor's Notes

  1. As a reminder, table 14-6 in Smeltzer outlines briefly the major anions and cations and their resulting states. Na concentration range is 135-145. Because Na does not permeate the cell wall easily, alterations in Na account for the alterations in water or fluid balance.
  2. Normal ionized calcium is generally accepted as between 4.5 – 5.5. Ionized calcium is the only form of calcium that is physiologically relevant. Serum calcium is frequently reported and must be adjusted for albumin levels and serum proteins.
  3. Both hypocalcemia and hypercalcemia are fairly common because so many factors influence Ca regulation. Ca is required for bone and teeth strength and density, blood coagulation, and nerve contraction. Ca is absorbed and utilized in the presence of vitamin d, and is controlled by PTH.
  4. Mg plays a great role in electrolyte balance as it is the second most abundant intracellular cation. As Mg plays a role in nerve conduction, Mg affects the cardiovascular system peripherally by producing vasodilation. Mg is also thought to decrease total peripheral resistance.
  5. 85% of PO4 is located in bones and teeth, with 14% in soft tissue, and less than 1% in ECF. PO4 levels decrease with age.