Electrolytes Flashcards
(29 cards)
Sodium Range
135-145 mEq/L
<135 hyponatremia
>145 hypernatremia
Potassium Range
3.5-5.0 mEq/L
<3.5 hypophosphatemia
>5.0 hyperphosphatemia
Calcium Range
8.5-10.5 mg/dL
<8.5 hypocalcemia
>10.5 hypercalcemia
> 15 hypercalcemic crisis
Magnesium Range
1.8-2.6 mg/dL
<1.8 hypomagnesemia
>2.6 hypermagnesemia
Phosphorus Range
2.5-4.5 mg/dL
<2.5 hypophosphatemia
>4.5 hyperphosphatemia
Bicarbonate (HCO3-) Range
22-26 mEq/L
<22 acidic
>26 basic
pCO2 (reversed)
35-45 mmHg
> 45 acidic
<35 basic
pH
7.35-7.45
<7.35 acidic
>7.45 basic
pO2
80-100 mmHg
Hypotonic Hyponatremia
Na < 135 mEq/L
dilution from water retention (SIADH)
retention of water with dilution of sodium while maintaining the effusive circulatory volume within a normal range
excessive sweating, loss of sodium and water, GI losses, heart failure
Hypertonic Hyponatremia
Na <135 mEq/L
resulting from an osmotic shift of water from ICF to FCF
sodium in the ECF becomes diluted as water moves out of body cells in response to osmotic effects of the elevated blood glucose level
occurs with hyperglycemia
Hyponatremia
Causes:
- excessive sweating (loss of NA and water)
- GI losses
- Heart Failure
- Hyperglycemia
Symptoms:
* neuromuscular excitability increased at first, then decreased * muscle cramps * N/V * Diarrhea * HA * Confusion * Disorientation * Lethargy, seizures, coma
Hypernatremia
Na >145 mEq/L and Serum Osmolality >295
Hypertonicity of ECF and intracellular dehydration
movement of water out of ICF (cells shrink)
Caused by: disproportional loss of body H2O in relation to Sodium
Symptoms:
* decreased neuromuscular excitability * agitation, headache, seizures, coma * decreased skin turgor * decreased secretions * decreased sweat/urine * fever
People at Risk for Hypernatremia
infants, the elderly and developmentally delayed are at risk, anyone that cannot speak for themselves, and people with kidney failure or tube feeds (can’t tell when they’re thirsty)
Why is Potassium so important?
- Maintains intracellular osmolality
- maintains acid-base balance
- changes glucose into glycogen
- convert amino acids into proteins
- CRITICAL in conduction of nerve impulses and muscle excitability
Hypokalemia
K <3.5 mEq/L
Causes: inadequate dietary intake, excessive renal losses, kidney excretes too much K, ECF to ICF shift, diarrhea
Symptoms: decreased NM activity, weakness, paresthesia, cramping, arrhythmias, cardiac arrest
Hyperkalemia
K >5.5 mEq/L
Causes: ICF to ECF shift, potassium has come out into the blood and concentration increases, decreased renal elimination (renal failure is the biggest cause), excessive oral or IV administration
Symptoms: (first) increased NM excitably, (severe) decreased NM excitability, neuro-parasthesia, paralysis, muscle weakness, CV (ECG changes, peaked T waves (mild) or lethal arrhythmias and cardiac arrest (severe)
Hyperkalemia raises resting potential toward threshold, cells fire more easily, mild hyperkalemia symptoms then severe
Hypoparathyroidism
deficient PTH secretion
Causes: congenital, autoimmune (destroy gland), surgery, hypomagnesemia
Manifestations: same as hypocalcemia
Causes: Renal failure (kidney losses), hypoparathyroidism, hyperphosphatemia, protein binding and chelation
Manifestations: Increased NM excitability, decreased cardiac excitability
neuro: paresthesia, muscle spasms, tetany, hyperactive reflexes
Chvostek’s and Trousseau’s Sign
CV: hypotension, HF, cardiac arrhythmia
Skeletal: chronic fractures
Electrolytes: Low serum ionized Ca
Hyperparathyroidism
causes: (primary) hyperplasia, adenoma or CA of gland
(secondary) chronic renal failure and chronic malabsorption of Ca
Manifestations: same as hypercalcemia
decreased NM excitability and muscle function, increased cardiac excitability
Neuro: lethargic, behavioral changes
CV: HTN, increased contractility, dysrhythmias
GU: renal calculi
Electrolytes: high Ca levels and renal osteodystrophy
Hypocalcemia
Ca <8.5
Causes: Renal failure (kidney losses), hypoparathyroidism, hyperphosphatemia, protein binding and chelation
Manifestations: Increased NM excitability, decreased cardiac excitability
neuro: paresthesia, muscle spasms, tetany, hyperactive reflexes
Chvostek’s and Trousseau’s Sign
CV: hypotension, HF, cardiac arrhythmia
Skeletal: chronic fractures
Hypercalcemia
Ca >10.5
Causes: hyperparathyroidism, cancer
Manifestations: decreased NM excitability and muscle function, increased cardiac excitability
Neuro: lethargic, behavioral changes
CV: HTN, increased contractility, dysrhythmias
GU: renal calculi
ABOVE 15, hypercalcemic crisis
Calcium
kidneys convert Vitamin D from the skin into the active form of Vitamin D which goes into the intestine and causes your system to absorb calcium
without Vitamin D the body cannot absorb calcium
exerts an important effect on membrane potentials and neuronal excitability
participates in the release of hormones
necessary for the contraction in skeletal, cardiac and smooth muscle
influences cardiac contractility and automaticity by way of slow calcium channels
Vitamin D
activation occurs in the kidneys and it effects the absorption of calcium
without vitamin D calcium cannot be absorbed by the body
Kidney Failure: Vit D not activated, calcium continuously secreted but unable to be absorbed, taken from bone instead
Hypophosphatemia
Causes: intentional absorption renal losses corticosteroids antacids malnutrition increased PTH chronic alcohol use
manifestations:
decreased NM excitability and muscle function, increased cardiac excitability
Neuro: lethargic, behavioral changes
CV: HTN, increased contractility, dysrhythmias
GU: renal calculi
