Electrolytes

Cations

Positive electrolytes = -ium

• Magnesium: 1.5-2.5 mEq/L

• Potassium: 3.5-5.0 mEq/L

• Calcium: 4.5-5.5 mEq/dL or 9-11 mg/dL

• Sodium: 135-145 mEq/L

Anions

Positive electrolytes = -ide

• Phosphorus: 2.5-4.5 mg/dL

• Chloride: 97-107 mEq/L

K+, P-

What are the intracellular electrolytes

Na+, Cl-

What are the extracellular electrolytes

1.5-2.5 mEq/L

Normal Values: Magnesium

3.5-5.0 mEq/L

Normal Values: Potassium

4.5-5.5 mEq/dL or 9-11 mg/dL

Normal Values: Calcium

135-145 mEq/L

Normal Values: Sodium

2.5-4.5 mg/dL

Normal Values: Phosphorus

97-107 mEq/L

Normal Values: Chloride

POTASSIUM

• Largest cation in your cells

• 98% of your potassium is in your cells

• 2% in your blood

• Regulated by Aldosterone (inverse relationship with K+)

  • Aldostrone → Na retention, water retention, potassium excretion

• Inverse relationship with Calcium

Cardiac contractility

function of K

High K+ Foods

Carrots, cantaloupe

Red meat, raisins

Orange, organ meat, avOcado, tOmato, pOtato

Watermelon

Dried fruits, dates, dark green leafy vegetables, dairy

Saging, spinach, Salt substitutes

Low K+ Foods

B - all with “berry”

Eggs

Red apples

Rice

Iceberg lettuce (light colored veggies)

Eggplant

Squash, shrimps (white meat)

Causes of hypokalemia

K+ wasting diuretics (loop, thiazide), laxatives

Insulin, sodium bicarbonate = blood to cell shifting

High aldosterone (Cushing's)

Fluid loss: vomiting, diarrhea, diaphoresis, diuresis

Burns (intermediate phase)

Alkalosis

Hypokalemia

MOST CRITICAL ELECTROLYTE IMBALANCE

Post op

Bulimia nervosa

Stress - increase cortisol - aldosterone causes decrease K+

decrease K+ intake

K+loss

Blood to cell shifting

S/Sx of hypokalemia

All s/sx are down except urine output

Lethargic

Low RR

limp muscle

Constipated (possible paralytic ileus)

Increase urine output

Bradypnea

Prolonged PR

ST depression

T wave flat/inverted

Prominent U wave

ECG changes in hypokalemia (PST-U)

Hypokalemia Management

K+ sparing diuretics: Spironolactone, Amiloride

K+ containing solutions

KCl

• oral with juice

• IV never push

• diluted in PNSS

• via pump only

K+sparing diuretics

Spironolactone, Amiloride, Triamterene, Eplerenone

up to 40 mEq/L

safe concentration of KCl

renal function

What will you monitor when administering KCl

5-10 mEq/hr

Safe infusion rate of KCl peripheral

10-20 mEq/hr

Safe infusion rate of KCl central

• With CARDIAC MONITORING

• WOF KCl toxicity

all are up except HR and UO

s/sx of hyperkalemia

management for KCl toxicity

• Stabilize patient’s heart

• Shift K+ (blood to cell)

• Eliminate K+

Calcium gluconate, calcium chloride

KCl toxicity medications

• to counteract the effect of hyperkalemia (calcium calms your nerve)

Kayexalate

last DOC in KCl toxicity

takes 4-6 hrs to act

K+ wasting diuretics

KCl toxicity medications: furosemide

Insulin with dextrose (D10W)

Sodium bicarbonate

KCl toxicity other medications

causes of hyperkalemia

• Drugs

  • K+ sparing “SEAT”

  • ACE and ARB

  • KCL

• Acidosis

• Cell lysis (aged/old blood)

  • Tumor lysis syndrome (chemo)

  • Crush injuries (vehicular accident)

  • Sickle cell disease

• Hypoaldosteronism (Addisson’s disease)

• Intake excessive (CROWDS)

• Nephron damage (CKD, KI)

  • All electrolytes are up except calcium

  • Emergent phase of burn injury/resuscitative (high K+, low Na)

hyperkalemia

increase K+ intake

K+ retention

Cell to blood release

S/Sx of hyperkalemia

All s/sx are up except urine output and HR

• Anxiety

• Hyperactive DTR

• Hypermotility of GI (diarrhea)

• Bradycardia

• Oliguria

Flat P

Widened QRS

Tall T wave

ST elevation

Hyperkalemia ECG changes (PQRST)

K+ wasting diuretics (loop)

Avoid K+ containing food

Calcium gluconate

Hyperkalemia management

Sodium

Mainly located at the brain

Fluid balance (regulates your BP)

Directly proportional relationship with Aldoserone

High Sodium Sources

Table salt

Processed food

Junk food

Smoked/cubed food

Pickled

Hyponatremia Causes

DASH/bland diet

Fluid overload → Na dilution → CHF, water intox, oxytocin, SIADH

Addison's

Diuretics (thiazide), hypotonic solutions (especially D5W)

thiazide

Most hyponatremic diuretic

Low → K+, Na+

High → Ca+, glucose, uric acid

oxytocin

hormone produced by PPG giving ADH-like effect → retention → fatal hypotension

shock

Manifestation of hyponatremia

true Na loss → true water loss

fluid overload

Manifestation of hyponatremia

Water gain (retention) → dilute Na → decreased Na

cerebral edema

complication of hyponatremia that could lead to increased ICP

Hypertension, bradycardia, bradypnea

Cushing’s triad for increased ICP

S/sx of increased ICP

Hyper-brady-brady

Widened pulse pressure (SBP-DBP) (>40 mmHg)

Bounding pulse (+4)

Hyperthermia (>40 degrees)

Dilated pupils/papilledema (dilated optic disk)

prevention of increased ICP

• Semi-fowler’s position (30 degrees)

• Lower environmental stimulus: lessen light, limit visitor

• Avoid straining (Avoid valsalva maneuver)

  • Stool softener 

  • Antitussive (Butamirate citrate)

mannitol

osmotic diuretic used to manage increased ICP

Hypertonic Saline solution (>0.9 NaCl)

IVF for increased ICP management

Gradual increase of Na

Prevent Osmotic Demyelination Syndrome

Osmotic Demyelination Syndrome

rapid removal of fluids in the cell

respiratory failure

If your brain cell including medulla and pons is dehydrated, it will cause

Seizure Precautions: Airway

Airway:

• Remove dentures, retainers

• ET tube, suction, tracheostomy (do this after)

• No padded tongue blade anymore

• NPO during

• Put them in a lateral position

Breathing:

• Oxygen + bag valve mask

Safety:

• Bed at lowest

• Siderails up with padding except infants due to increased risk of SIDS

• Cushion the head

• Do not restrain

increased salt intake, PNSS, tolvaptan and declomycin

Management for hyponatremia

Hypernatremia Causes

Excessive sodium intake

Sodium retention

• CKD

• Cushing’s

Hemoconcentration (ADH)

Hypertension, thirst, thick secretions

S/sx of hypernatremia

brain cell dehydration, seizures

Hypernatremia complications

herbs and spices

substitute for salt (management for hypernatremia)

D5W

IVF for hypernatremia

Increase fluids, desmopressin

management for hypernatremia = DI

Clotting, cardiac contractility, calms nerves

Functions of calcium

Calcitonin

Calcium is regulated by?

tones down calcium (blood to bone)

osteoblast (build your bone)

• Reabsorption

  Mineralization

PTH

Calcium is regulated by?

bone to blood

Osteoclast

Bone resorption (losing the calcium) / demineralization

Calcitriol

Calcium is regulated by?

active Vit D (from kidney)

direct

relationship of magnesium and calcium

Causes of hypocalcemia

Low Ca intake

HypoPTH, hyperphosphatemia

Alcoholism, malabsorption (Celiac, Crohn's), pancreatitis

gluten

what food is contraindicated to patient’s with celiac’s dse

• Tetany 

• Chvostek’s sign -  tap cheeks

• Trousseau’s  - BP cuff

  • Carpopedal spasm (flex))

  • Clonus (hyperactive, severe, +4)

• Cardiac dys

• Seizures

• Bleeding (low calcium level)

laryngospasm

WOF in tetany

tingling of mouth

1st sign of hypocalcemia

Carpopedal spasm

a condition characterized by involuntary, painful contractions of the muscles in the hands and feet, and sometimes the wrists and ankles associated with hypocalcemia

Trousseau’s

Flex

Calcium supplements, Calcitriol, calcium gluconate

Management of hypocalcemia

Causes of Hypercalcemia

HyperPTH, immobility, glucocorticoids

Hypophosphatemia, calcium meds (TUMS, antacids), malignancy

S/Sx of hypercalcemia

Respiratory failure

Clotting

Low bone calcium

Fracture

Renal calculi

Management for hypercalcemia

Increase fluids, PNSS

Loop diuretics (not thiazide)

Calcitonin