Lyte Imbalance Flashcards
Extended chemistry Panel includes
Calcium, phosphate Mg, in addition to usual chemistry panel
Hypernatremia
Occurring bc of water loss or Na Gain
Causes hyperosmolality leading to cellular dehydration
Primary protection is THIRST from hypothalamus
Does not normally occur in pts with norma LOC who can sense thirst and swallow
Manifestations of Hypernatremia
Intense thirst
Lethargy
Agitation
Progressing to Seizures (maybe)
Coma
Due to Dehydration of the neurons
Treating hyernatremia
Treat the cause
- treating reason for dehydration
- Giving drink OR isotonic solution to dillute sodium
Primary water deficit? PO or IV 0.9% NaCl
Primary sodium excess? Dilute w/ salt-free IV fluids (ie D5W) & excrete Na+ w/ diuretics
Serum sodium levels must be reduced gradually to avoid cerebral edema IMPORTANT
Hyponatremia causes
Occuring due to water gain, or sodium loss or both
Inappropriate use of sodium-free or hypotonic IV fluids
SIADH (Syndrome of Inappropriate ADH) - dilutional hypoH connected to water retention
Losses of sodium-rich body fluids from the GI tract, kidneys and skin (ie sweat)
Manifestation of hypoNa
Due to cellular swelling in CNS
Altered CNS:
Headache
irritability
confusion/conc difficulty
Seizure
coma
Likely Progressive
Treatment of hypoNA
Fluid restriction
Increases conc of Na in blood
Hypertonic saline VERY extreme - pt would have REALLY altered LOC, potentially comatos
Severe K+ deficit or excess we are most worried abt
Myocardial contractility
- Can lead to SIGNIFICANT dysrythmias
Less than 3, greater than 6.5-7
K+ is necceassry for
Transmission and conduction of nerve impulses
Maintenance of cardiac rhythms ***
Skeletal & smooth muscle contraction
Acid–base balance
Factors that cause Na retention cause Potassium _____
Depletion/loss
e.g. low blood volume, increased aldosterone)
Primary organ dealing with K+ balance
Kidneys 90% responsible
CKD can result in HyperK
Causes of hyper K
Massive intake
Renal failure
Shift from intercellular fluid to extracellular fluid (acidosis)
Massive cell destruction (crushing, ischemia, burns)
Catabolic states
Transfusion of aged blood
Acidosis and hyper K
Too much K in cells means that H+ is pulled into bloodstream
Manifestations of hyperK
Weak or paralyzed skeletal muscles
May experience cramping leg pain
Ventricular fibrillation or cardiac standstill
Abdominal cramping or diarrhea
Normal K is high intercellular and low extracelular causing negative electrical membrane - increase K = decrease excitablilty
Nursing management of hyperKalemia
C - Calcium Gluconate (stablize myocardium)
B - Beta2 Adrenergic Agonist (Salbutamol) - bronchodilator
I - Insulin - Moves glucose into cells AND K+ into cells
G - Glucose
K - Kayxalate - Binding Resin working in GI tract, sustain lower level
Drop - Diuretics (Loop or Thirazide)
- Require functional kidneys
- Dialysis
If pt levels of K are below 3 and over 7 nursing interventino
Cardiac monitering
Causes of HypoK
Abnormal Losses of K by kidneys or GI tract
Shift from extracellular to intercellular
Inadequate intake (rare)
Diuretic use
*Magnesium deficiency**
- Mg and K are correlated
Metabolic alkalosis
Hypokalemia Manifestations
Most serious are cardiac
(Depolarization of cell membranes)
Skeletal muscle weakness & paralysis
Muscle cramping & muscle cell breakdown
Not important
Decreased GI motility (paralytic ileus)
Diuresis
Hyperglycemia
Hypokalemia management
Supplements given PO or IV (IV if needing rapid), but PO is still quickly absorbed
Should not exceed 10-20mmol/hr of replacement
IV K+ must always be dilluted in IV fluid
Calcium obtained by
Ingested foods
More than 99% combined with phosphorus and concentrated in skeletal system
Ca and Phospherus relationship
Inverse
Primary storage of Ca
Bones - therefore, in dficiencies, bones and teeth are demineralized to increase serum levels
What does Ca do
Blocks sodium transport and stabilizes cell membrane
Ionized form is biologically active
3 ways in which the blood carries Ca (Not super important)
Free or ionized form (Biologically active)
- Availble to do the work, not stored
Bound to protein (Albumin mainly)
- Low levels of albumin causes issues
Complexed with phosphate citrate or carbonate
Changes in serum pH affect on Ca
Acidosis decrease Ca binding to albumin = increase Ca levles
Alkolosis is opposite
Calcium functions
Transmission ofnerve impulses
Myocardial contractions
Blood Clotting
Formation of teeth and bones
Involved in muscle contractions (controlled by PTH INCREASES resorption and calcitonin decreases RESORPTION)
Calcitonin
Produced by thyroid gland
Stimulated by high serum hormones
Lowers CA lelve by deceasing GI absorption, promoting rneal excretion and resorption into bones
HyperCa caused by
Hyperparathyroidism
Malignancy in the bone (seconadary to breast and lung cancer)
Not important
Prolonged immobilization
Manifestations of Hyper Ca
Cardiac dysrythmias
Neuro alterations
Not important
Mood changes
Neuron death
Decreased memory
Alterations in mental function/confusion/disorientation
Fatigue
Bone Pain
Renal Calculi (Kidney stones)
Nursing implications for HyperCa
Promote excretion of Ca in the urine
- Drink 3-4L a day
- IV saline bolus (More immediate)
- Loop diuretic
Sustaining w/ Synthetic calcitonin (Nasal spray, injection)
Sustaining with low Ca diet
Mobilization - wt bearing activities
IV Pamidronate (In malignancy)
- Reverse levels quickly
HypoCa Caused by
Hypoparathyroidism
Chronic alcoholism or hypoalbuminemia (liver disease)
Acute pancreatitis
Malabsorption syndromes & diarrhea (e.g. Crohn’s disease)
Multiple blood transfusions
Inadequate dietary intake
Low Ca or Vit. D intake
Medications
Steroids
Loop diuretics (e.g. Lasix)
Laxative abuse
Manifestations of hypoCa
Depression, anxiety, confusion
Tetany
Numbness & tingling in extremities & region around mouth
Positive Chvostek’s or Trousseau’s sign
Dysphagia
Laryngeal stridor
Hyperreflexia, muscle cramps
Seizures
ECG changes
Positive Chvostek’s or Trousseau’s sign
Arm contraction during BP (Trousseaus)
Twinging front of ear causing a facial twitch (Chvostek)
Nursing management of HypoCa
Treat cause
PO/IV supplements
Ca Rich Diet/ Vot D supplements
Phosphate
Primary anion in the ICF (along with K+)
Essential to the function of:
Muscle
RBCs
Nervous system
Involved in:
acid-base buffering system
Mitochondrial energy production of ATP
Cellular uptake and use of glucose
Metabolism of carbohydrates, proteins and fats (as an intermediary in)
Inverse relationship between PO4 and Ca2+
Renal function must be adequate to maintain normal levels of PO4
Hyperphosphatemia
Acute or chronic renal faiulre **
chemotherapy
Excessive ingenestion of milk or phosphjate containing laxatives
—-
Manifestations of hyperPhosph
Hypocalcemia
Muscle problems / tetany
Deposition of calcium-phosphate precipitates in skin, soft tissue, corneas, viscera, blood vessels
Management of hyperPhosph
W/ renal funciton
Don’t eat too much phospherus
Ensure adequate hydration and correction of hypoCa conditions
W/ Renal Failure
Dietary phosphate restrictions
–
–
Hypophosp manifestations
Changes in mental status
CNS depression
Confusion
Muscle weakness
Pain
Dysrythmias
Nursing management of Hyophosph
Mild- oral supplementation
Severe - IV supplementation (Rare)
- Dangerous with causing precipitate in BV
Mg Important for
Second most abundat intracellular Cationafter K+
Required for production of ATP
Muscle contration and relaxation
- Less critical for cardiac, but more involved in mental and cog chagnes and skeletal muscles
Factors that regulate calcium (ie PTH) seem to influence magnesium as well
Because magnesium balance is related to K+ and Ca2+, they should be assessed together
Know Phosphate AS it pertains to CA (KNOW Ca first)
Mg is related to
Ca
HyperMg
Increased intake
Renal insuffeciency
Combo of both
Pts on Lithium
Manifestations of hypermg
Nerve and muscle function impairment
HOTN
Facial flushing
Lethargy
urinary retention
As it progresses
Deep tendon reflexes loss
Muscle paralyis
Coma
Resp depression
