Fluid and Electrolytes revisited Flashcards
Major Cations
sodium, potassium, calcium, magnesium, hydrogen
Major Anions
chloride, bicarb, phosphate, sulfate, proteinate
non electrolytes
BUN, Creatinine, Glucose
Major Electrolytes of ECF
Na+ (most important)
Cl- (important)
Ca 2+
HCO3- (important)
Major Electrolytes ICF
K+ (most important) Phosphate- Sulphate- Protein - Mg+ (important)
Normal Sodium Plasma levels
135-145 mEq/L
Sodium balance
Sodium is most abundant ECF cation
Key to ECF volume
Diffuses between vascular and interstitial fluids (ECF)
Quickly transported OUT of cells by ATP-ase pump
Roles of Sodium
key to establishing transmembrane potential in all living cells
participates in action potential of excitable cells/tissues
critical to normal neuron, brain, muscle function
actively secreted in mucous and other secretions
comprises about 90% of osmotic forces
Sodium levels reflect…
WATER BALANCE
Serum sodium less than 135 mEq/L..?
Hyponatremia- TOO MUCH WATER
Causes of hyponatremia
losses from excessive sweating, vomiting, diarrhea, diuretic abuse
certain diuretic drugs combined with low salt diets
hormonal imbalances (insufficient aldosterone, adrenal insufficiency, excess ADH secretion/SIADH
excessive water intake
Effects and Clinical Manifestations of Hyponatremia
fluid imbalance in compartments –> fatigue, muscle cramps, abdominal discomfort, nausea, vomiting
Decreased osmotic pressure in ECF = cells swell
cerebal edema
neurological changes - headache, weakness, confusion, seizures, even coma and death
poor skin turgor, dry mucosa, decreased salivation
nausea, abdominal cramping
hypovolemia and decreased BP (all fluid going to CELLS)
Management of hyponatremia
treat underlying condition
medicate
assess: I + O, daily weight, lab values, CNS changes
encourage dietary sodium
evaluate effects of medications (diuretics, lithium)
maybe…:
replace sodium
restrict water
hypertonic saline
Serum sodium greater than 145 mEq/L
Hypernatremia = WATER DEFICIT
most affected are very old, very young, cognitively impaired
Potential causes of hypernatremia
fluid deprivation excess sodium administration diabetes insipidus heat stroke hypertonic IV solutions insufficient ADH = dilute urine loss of thirst mechanism water diarrhea prolonged rapid respiration without adequate fluids large amt of sodium ingested w/o water
Effects and Clinical Manifestations of Hypernatremia
cells shrink
increased thirst weakness,agitation elevated temp dry, rough mucous membranes Edema (fluid moves into ecf) increased BP (maybe)
Management of Hypernatremia
Gradual lowering of serum sodium level via infusion of hypotonic electrolyte solution
(oral fluids ok w/ alert pt and safe to swallow)
diuretics
assessment for abnormal loss of water and low water intake
assess for OTC sources of sodium
Monitor for CNS changes
Normal Potassium Serum Levels
3.5 - 5.5 mEq/L
Potassium balance
one of most imporant minerals in body
most abundant intracellular cation
30x higher in cell than out
Assessing K+ routinely done in INPATIENT settings
difficult to assess K+ levels since most are in cell
Blood potassium is often poorly indicative of tissue potassium stores
Importance of Potassium
primary ion that establishes normal transmembrane potential in all living cells
participates in action potential
maintains normal electrical activity of excitable cells
critical to normal neuron, brain, and muscle function (including HEART, smooth muscle, skeletal muscle)
maintains ICF volume
critical to normal renal function
strong relationship with sodium
Potassium serum level less than 3.5 mEq/L
Hypokalemia
may occur with alkalosis as serum potassium goes INTO cells and H+ goes OUT
Causes of Hypokalemia
excessive potassium loss in urine due to prescription medications that increase urination (ie: loop diuretics)
poor dietary intake
alterations of acid-base balance
Clinical Manifestations of hypokalemia
ECG changes
dysrhythmias
muscle weakness
decreased bowel motility
paresthesias
dilute urine
excessive thirst
fatigue
anorexia
Management of Hypokalemia
Potassium replacement
Dietary or IV (if deficit severe)
slow rate of K+ administration, no faster than maximal rate
Slowly w/ infusion pump and only have adequate urine output has been established
What to monitor for when treating hypokalemia
ECG for changes
ABGs
Receiving digitalis for toxicity
early signs and symptoms
Serum potassium greater than 5.0 mEq/L
Hyperkalemia
seldom occurs in pts with normal renal function
increased risk in older adults
CARDIAC ARREST is frequenly associated
Causes of hyperkalemia
Impaired renal function
MED ERROR: too rapid admin of K+
HYPOaldosteronism: aldosterone functions to move K+ into cells of kidneys to be excreted. low aldosterone activity = increased K+ levels
meds, tissue trauma, tumor lysis syndrome, acidosis (H+ enters cell, K+ leaves)
Clinical Manifestations of hyperkalemia
Cardiac changes
dysrhythmias
muscle weakness
paresthesias
anxiety
GI problems
Management of Hyperkalemia
Monitor ECG
assess labs
monitor I+O
obtain apical pulse (rhythm and rate)
Limit dietary potassium
Administration of cation exchange resins (Kayexalate)
Emergent care of Hyperkalemia
IV calcium gluconate
IV sodium bicarb
IV regular insulin and hypertonic dextrose IV
beta 2 agonists
dialysis
administer IV slowly and w/ infusion pump
Normal Serum Levels of Calcium
8.8-10.5 mg/dL
Calcium balance
most abundant mineral in whole body
serum calcium is very tightly regulated and does NOT fluctuate with changes in dietary intakes
bone tissue used as reservoir for calcium to store it and maintain constant concentrations in blood, muscle and ICF
Importance of calcium
normal neuron signaling
MUSCLE CONTRACTION
used as intracellular second messenger
essential for neurotransmitter secretion; ALL muscle contractions (heartbeat, vasoconstriction and dilation, skeletal and smooth muscle)
hormonal secretion
intracellular signaling
hemostasis
a SMALL AMT. of calcium is needed to support these metabolic functions
Calcium and bone
remaining 99% of calcium supply stored in bones and teeth where it supports structure and function
bone goes under constant resorption and deposition of calcium throughout life
more deposition in youth, even in adults, more bone breakdown in older adults
Serum calcium level controlled by…
Parathyroid hormone
raises serum calcium levels –> activates osteoclasts –> increasing reabsorption from intestines and renal tubules
lowers serum calcium levels –> inhibits osteoclast activities –> inhibits reabsorption of calcium from renal tubules
calcitonin
Calcium serum level less than 8.6 mg/dL
Hypocalcemia
must be considered in conjunction with serum albumin level
why?: calcium ion highly bound to proteins, cannot be interpreted w/o total protein/albumin level
Causes of hypocalcemia
hypoparathyroidism
malabsorption
osteoporosis
pancreatitis
alkalosis
transfusion of citrated blood
kidney injury
medications
Clinical manifestations of hypocalcemia
tetany
circumoral numbness
paresthesias
hyperactive deep tendon reflexes
Trosseau sign
Chovostek sign
seizures
respiratory symptoms (dyspnea and laryngospasm) abnormal clotting
anxiety
Management of hypocalcemia
IV calcium gluconate (emergent situations)
Seizure precautions
oral calcium and vitamin D supplements
exercises to decrease bone calcium loss
patient teaching for diet and meds
Chvosteks Sign
signs of tetany
abnormal rxn of facial nerve
tap at angle of jaw (masseter muscle) –> muscles of face will twitch momentarily due to hyper excitability of nerves
Trosseau Sign
cramping of hands w/ BP cuff on
Calcium serum level greater than 10.2 mg/dL
Hypercalcemia
high mortality
Causes of Hypercalcemia
malignancy
hyperparathyroidism
bone loss related to immobility
diuretics
Clinical Manifestations of Hypercalcemia
polyuria
thirst
muscle weakness
intractable nausea
abdominal cramps
severe constipation
diarrhea
peptic uler
bone pain
ECG changes
dysrhythmias
Management of hypercalcemia
treat underlying cause
administer IV fluids (furosemide, phosphates, calcitonin, bisphosphates)
increase mobility
encourage fluids
dietary teaching
fiber (for constipation)
ensure safety
