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Electrolyte Homeostasis & Imbalances

NRS 232 - Pathophysiology I
by

Katrina Dielman

on 26 January 2016

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Transcript of Electrolyte Homeostasis & Imbalances

Electrolyte Homeostasis & Imbalances
Overview of Electrolyte Homeostasis & Imbalances
Magnesium
2 Forms constitute serum magnesium (1.5-2.5 mEq/L):
Bound - inactive
Unbound - "Free Ionized" -
physiologically active
Potassium
Potassium influences cellular membrane
resting potential
Calcium
Hypocalcemia
Decreases
the
threshold potential
of nerve and muscle cells causing
hyperexcitability
Hypercalcemia
Causes/Risk Factors
Clinical Assessment
-

Prioritize!
Electrolytes:
Ionized salts dissolved in water
Most clinically important:
Sodium
Potassium
Calcium
Magnesium
Chloride
Bicarbonate
Phosphate

Electrolytes - Normal Levels

Concept Map of
Crucial Interrelationships
The
plasma concentration
may not reflect the
intracellular concentration
!
Intracellular
space contains higher concentrations of:
Potassium
Calcium
Magnesium
Phosphate

Extracellular
fluid contains higher concentrations of:
Sodium
Chloride
Bicarbonate
3 Forms constitute "Total Calcium" (9-11 mg/dL):
Bound to plasma protein (albumin) - inactive
Bound to small organic ions (citrate) - inactive
Unbound - "Free Ionized" -
physiologically active
4-5 mg/dL
Distribution
between the electrolyte pool and extracellular fluid is largely influenced by
parathyroid hormone (PTH)
Causes/Risk Factors
Clinical Assessment
- Prioritize!
Teaching
Teaching
A. Normal
B. Hypomagnesemia
C. Hypermagnesemia
Hypomagnesemia
Hypermagnesemia
Hypokalemia
Hyperkalemia
References
Calcium
influences the
threshold potential
of
nerve
and
muscle cells
Twitchy!
Increases
the
threshold potential
causing
hyporeflexia - neuromuscular depression
Floppy!
Increases
neuromuscular excitability
Twitchy!
Depresses
neuromuscular excitability
Floppy!
Causes
hyperpolarization
Skeletal muscle weakness
Flaccid paralysis
Cardiac dysrhythmias
Skeletal muscle weakness
Flaccid paralysis
Cardiac dysrhythmias
Causes
hypopolarization
Distribution
between the electrolyte pool and extracellular fluid is largely influenced by
epinephrine
and
insulin
Magnesium ions in the extracellular fluid normally
depress
the release of
acetylcholine
at
neuromuscular junctions
Serum potassium (3.5-5.0 mEq/L)
normally reflects only the small portion of extracellular potassium - May not reflect the total body potassium
Causes/Risk Factors
Clinical Assessment
- Prioritize!
Teaching
Copstead, L. & Banasik, J. (2013).
Pathophysiology
(5th ed.). St. Louis, MO: Elsevier.

Felver, L. (2013). Online Materials:
PROP- Pathophysiology online.
Retrieved from https://evolve.elsevier.com/

Giddens, J. (2013).
Concepts for nursing practice
(1st ed.). St. Louis, MO: Elsevier Mosby.
Normal output but deficient intake/absorption
Diet lacking Ca++ rich foods
Poor Ca++ absorption (
diarrhea, lack of Vit. D
)
Increased output via GI tract
Steatorrhea
binds Ca++ in GI secretions, as well as dietary Ca++
Ca++ shift from ECF into bone or physiologically unavailable form
Hypoparathyroidism
Large load of
citrate from massive blood transfusion
- binds the Ca++
Alkalosis
(causing more binding to albumin) or elevated plasma phosphate level
Acute
pancreatitis
- Ca++ binds to necrotic fat in the abdomen
Increased neuromuscular excitability
+ Chvostek's and Trousseau's signs
Muscle cramps
Twitching
Hyperactive reflexes
Carpal/pedal spasms
Tetany
Seizures
Laryngospasm
Cardiac dysrhythmias
Serum total calcium < 9 mg/dL
Almost always requires prompt reporting/intervention!
Prevent diarrhea from laxative abuse
If have chronic diarrhea or other risk factors for hypocalcemia, then increase calcium intake
Milk and dairy
Chocolate
Almonds
Canned fish with bones
Oranges/orange juice
Oysters
Tofu
Dark green leafy vegetables
If cannot tolerate dairy products, advise about other sources
Output less than excessive intake/absorption
Vitamin D or Ca++ overdose
Decreased output
Use of
thiazide diuretics
- affect transport of calcium in the tubules
Calcium shift from the bone into

ECF
Hyperparathyroidism
Cancers that secrete bone-resorption factors
Prolonged immobilization
Decreased neuromuscular excitability
Anorexia
Nausea
Constipation
Muscle weakness
Diminished reflexes
Decreased LOC
Cardiac dysrhythmias
Serum total calcium > 11 mg/dL
Avoid excessive Vitamin D supplementation
If hypercalcemic,
prevent renal damage
by drinking abundant fluids
3-4 liters/day
for adults
Goal:
Keep urine very dilute!
Causes/Risk Factors
Deficient intake or absorption
Diet lacking Mg++ rich foods
Poor Mg++ absorption -
chronic diarrhea
,
ileal resection
,
chronic alcoholism, malnutrition
Increased output
GI losses
Prolonged
vomiting
,
gastric suction
, or
draining GI fistula
Steatorrhea
- binds Mg++ in GI secretions, as well as dietary Mg++
Renal losses
Alcoholism,
loop & thiazide diuretics, uncontrolled diabetes mellitus, hypercalcemia
Acute pancreatitis
- deposition of Mg++ cation in areas of fat necrosis
Shift into physiologically unavailable form
Large load of
citrate from massive blood transfusion
- binds Mg++
Alkalosis
- more Mg++ binds albumin
Clinical Assessment
- Prioritize!
Increased neuromuscular excitability
+ Chvostek's and Trousseau's signs
Insomnia
Hyperactive reflexes
Muscle cramps
Twitching
Nystagmus
Tetany
Seizures
Cardiac dysrhythmias
Serum Magnesium < 1.5 mEq/L
Almost always urgent need to report/intervene!
Teaching
Prevent diarrhea from laxative abuse
Increase Mg++ intake if chronic diarrhea or malabsorption/other risk factors
Cocoa
Coffee
Egg yolk
Dark green leafies
Legumes
Meat
Milk
Nuts
Whole grains
Causes/Risk Factors
Output less than excessive intake/absorption
Overuse of
Mg++ containing laxatives/antacids
Decreased output
Chronic oliguric renal disease
Clinical Assessment
- Prioritize!
Decreased neuromuscular excitability
Flushing
Diaphoresis
Diminished reflexes
Hypotension
Decreased LOC
Muscle weakness
Respiratory depression
Bradycardia
Cardiac dysrhythmias
Serum Magnesium > 2.5 mEq/L
Teaching
Substitute another method of bowel regulation
for the use of mg++ containing laxatives
If have
oliguric renal disease
, carefully avoid use of mg++ containing antacids/laxatives
If hypermagnesemic, avoid intake of mg++ containing foods
Causes/Risk Factors
Deficient intake
Prolonged anorexia or diet lacking K+
NPO plus IVF lacking K+
Increased output
Vomiting
Acute or chronic
diarrhea
Use of
K+ wasting diuretics
or other drugs that increase K+ excretion
Excessive
aldosterone effect
- black licorice, cirrhosis, CHF, primary hyperaldosteronism
High levels of
glucocorticoids
- cortocosteroid therapy, Cushing's disease
Rapid shift from ECF into cells
Alkalosis
Excessive beta-adrenergic stimulation
Excessive
insulin
Clinical Assessment
- Prioritize!
Bilateral ascending flaccid muscle weakness
Abdominal distention
Constipation
Postural hypotension
Polyuria
Cardiac dysrhythmias
Serum potassium < 3.5 mEq/L
Teaching
Avoid extreme dieting
Prevent diarrhea
from laxative abuse
Increase K+ intake if have diarrhea or other risk factors
Apricots
Bananas
Cantaloupe
Grapefruit/Oranges
and their juices
Raisins
Strawberries
Asparagus
Beets
Broccoli
Excessive or too rapid intake
IVF with K+
at too rapid rate or excess amount
Massive transfusion of stored blood
(> 8 units)
Decreased output
Oliguria
- severe hypovolemia, circulatory shock, acute kidney injury, end-stage renal disease
Use of
K+ sparing diuretics
,
ACE-inhibitors
, or other drugs that reduce K+ excretion
Lack of aldsoterone
- adrenal insufficiency, Addison's disease
Rapid shift from the cells into ECF
Acidosis
Lack of insulin
Massive sudden cell death
- crush injuries, tumor lysis syndrome
Bilateral ascending flaccid muscle weakness
Cardiac dysrhythmias
Cardiac arrest
Serum potassium > 5.0 mEq/L
Dysrhythmias associated with hyperkalemia are among the most dangerous;
hyperkalemia requires urgent response!
If urine volume decreases, stop K+ containing preparations
Keep potassium supplements away from children!
If you have hyperkalemia or risk factors, decrease intake of K+ rich foods
NRS 232 - Pathophyisology I
Calcium Homeostasis
Symptom of preeclampsia:
Clonus
Treated with magnesium infusion
Mr. Postop
had a
thyroidectomy
2 days ago. He now reports fatigue and anxiety and states, “My hands are asleep, and I feel prickly pins around my mouth.” Mr. Postop has a history of goiter, hypertension, and anxiety.

His current medications are:

• Atenolol 50 mg PO daily for HTN – beta blocker
• Aspirin 81 mg PO daily to prevent MI/stroke – NSAID
• HCTZ/triamterene 1 capsule daily for HTN – thiazide diuretic
• Potassium chloride 20 mEq PO daily as supplement
Khan Academy:
Aldosterone lowers potassium
Mr. Hibeepee
, age 48, has high blood pressure. "I know I am supposed to eat a lot of potassium while I am taking these water pills, but I am afraid I'll gain weight from eating a banana with every meal. Is it better to get fat and keep my potassium up or keep from getting fatter and be low on potassium? What do you recommend that I do?" Answer as if you are speaking directly to Mr. Hibeepee.
"I told my nurse practitioner that I can't afford all these pills," says
Ms. Smallbudget
. "He said that if I can eat enough high-potassium foods, he will let me take fewer potassium pills. So tell me what those high-potassium foods are!" Answer as if you are speaking directly to Ms. Smallbudget
Mr. Primaryintention
has recovered from surgery that removed some of his small intestines, including most of his ileum. The cut ends were anastomosed and he is now eating solid foods again. "The doctor told me to eat foods that have a lot of magnesium, but she did not say why," he says. "She also said you would tell me which foods to eat for magnesium. What is this all about?" Answer as if you are speaking directly to him.
Ms. Changedlife
has chronic renal failure and will begin dialysis sessions this week. "The doctor said I should not use antacids like Maalox, but only the ones on this list," she says. "I have some Maalox at home. Why can't I just finish it before I buy a new kind? I do not want to waste money." Answer as if you are speaking directly to her.
Full transcript