Electrolyte abnormalities

Electrolytes

• substance that are electrically charged when they are in solution (cat ion: positive, an ion: negative)

What electrolytes are intracellular vs extracellular

• extracellular: Sodium (Na+), proteins-, Chloride (Cl-), Bicarb (HCO3-)(serum Co2 level)

• intracellular: potassium (K+), Magesium (Mg2+), sulfate (SO4-), phosphorus (PO4-), and proteins -

Electrolyte balance

• function together, if balance is disrupted in one electrolye, it can affect the others

• intake/ absorption/ distribution

• Excretion must be balanced in order to maintain homeostasis

Normal levels of Sodium

135-145

Normal levels for potassium

3.5-5

Sodium

• The most abundant cation in ECF

• determines osmolality (where Na is water follows)

• aids in acid-base balance

• activated muscle and nerve cells

• action potentials need Na in order to fire (Na rush into cell)

Hyponatremia

• low Na below 135

• more water than sodium in some cases, bottom line: sodium level in the blood is too low

• ECF fluid is low= diluted

• rapid changes and drops in Na is more symptomatic than slow decline

Hyponatremia continued

• beer potomania

  • ETOH intake chronically lowers Na due to low solute delivery to the kidneys

• excessive water intake (dilutes all the Na)

• water intoxication

  • replacing losses with just water: example drinking just water on a hot day when you are sweating (sweaty out salt and water so need to replenish both)

Two types of Hyponatremia

• Dilutional hyponatremia: total body Na near normal, total body water (same amount of Na but too much water) increased

  • hypervolemic (edema): heart failure, cirrhosis (liver), nephrotic syndrome

  • Euvolemic (no edema): SIADH, hypothroidism, secondary adrenal insufficiency

• Depletional hyponatremia Hypovolemic: Na lost, and total body water reduced

  • diarrhea, vomitting, burns, trauma, pancreatitis, diuretics, renal salt wasting, primary adrenal insufficiency

SIADH: syndrome of Inappropriate ADH

• inappropriately hold onto water, dilue Na levels

• Excessive ADH secretion (anti-diruretic hormone) kidneys hold onto water

• Hyponatremia with low serum osmolality

• Dehydrated (low volume) HR increased

Hyponatremia treatment

• treat underlying problem

• fluid restriction if volume overload (diuretics if indicated)

• Sodium replacement (Oral or IV; 0.9% NS solution)

• Severe symptomatic Hyponatremia: Not chroninc less than 125

  • usually in ICU

  • Increase Na by 1-2 mew every hour until symptoms improve

  • Telemetry monitoring

  • monitor neuro every 2-4 hours

Osmotic Demyelination Syndrome

• correcting hyponatremia too fast is common cause (can cause permanent damage)

• destruction of the myelin sheath is brainstem and pons

• Central Pontine Myelinolysis

  • acute paralysis: starting with weakness in face, arms and legs

  • Dysphagia: difficulty swallowing

  • Dysarthria: difficulty with speech

  • No know cure, treatment focused on symptom management

Hypernatremia

• too much Na compated to water, osmolality of ECF is high

• Na level past 145

Hypernatremia Causes

• Excess Na:

  • salt loading

  • medications

  • too much Na administration (Sodium bicarbonate is common drug that can do that )

  • many other medications in saline, Zosyn is one

• Water losses (most common)

• watery dirarrhea

• impaired thrist

• uncontrolled diabetes mellitus

• water deprication

• diuresis

• tube fedding without free water

• diabetes insipidus lack anitdiuretic hormone, so no conservation of H2O

Hypernatremia clinical manifestations

• thirst

• dry mucous membranes

• Oliguria (low urine, kidney try to hold onto water, means kidney is the issue)

• changes in neuro function: confusion, lethargy, seizures, coma

Hypernatremia Treatment

• correction of water deficit

• water deficit= 0.6 (weight in kg) X ([serum Na ÷ 140] -1)

• Replace ½ in first 24 hours

• D5W or free water orally or with tube feeding

Potassium

• 3.5-5

• Main intracellular ion

• regulates excitability of cells-cell electrical status

• helps control intracellular osmolality

Hypokalemia Causes

• level below 3.5

• K+ loss

  • decreased PO intake

  • Gi tract: stool output

  • Kidneys: normal loss or diuresis (main way of controlling K+)

• Shift from ICF to ECF

• acid-base abnormality

• Hydrogen ions move INTO the cells to correct an abnormally low pH (acidosis)

• K+ shifts in the opposite direction- out of the cells- to maintain electrical neutraluty

• when the pH is fixed the H+ and K+ will go back to where they started

Hypokalemia clinical manifestations

• Alkalosis

• Shallow respirations

• confusion, drowsiness

• Weakness, fatigue

• Arrhythmias- tachycardia, irregular rhythm and or bradycardia

• lethary

• thready pulese

• decrease intestinal motility nausea vomitting ileus

Hypokalemia treatment

• oral (safest)

• Potassium Chloride (KCl)

  • liquid, tabs or powder

  • causes GI upset

  • Also GI bleeding, dilute with lost of water. also do not give if pt. is NPO for OR

• Intravenous

  • must be given slowly and diluted

  • central line 20 Meq run over 1 hour

  • Peripheral IV 10 Meq

    • can cause pain/phlebitis

    • NEVER GIVE RAPID IV PUSH THIS CAN BE VERY BAD

Hyperkalemia Causes

• decreased output (most common)

  • kidney failure

  • massive cell injury: crush injury or muscle damage, K+ released on cell death

• Increase K+ intake

  • dietary or medically (K+ sparing diruetic→ spirnolactone)

• Shift from ICF to ECF

  • acid base abnormalitu

  • hydrogen ion move INTO the cells to correct an abnormally low pH (acidosis)

  • K+ shifts in the opposite direction- out of the cells- to maintain electrical neutrality

  • when the pH is fixed, the H+ and K+ will go back to where they started

  • Cation with succinlycholine administration can cause worsening HperK: 0.5-1.0

Hyperkalemia Clinical Manifestations

• Heart palpitations

• muscle weakness

• naseua and vomiting

• chest pain

• diarrhea

• arrhthmia

• abdominal pain

• Peaked T wave

Hyperkalemia Treatment

• Sub acutely

  • stop supplemental K+

  • limit K+ rich foods

• Cation exchange resin

  • sodium polystyrene sulfonate: oral or enema

  • Given infrequently because of adverse effects

    • intestinal necrosis has been reported

• Emergency: push K+ into the cells

  • Glucse (ampD50) and insulin (10 units IV) (push K+ into cells)

  • NaHCO3 (push H+ out and push K+ into cells)

  • Temporary treatment

• Dialysis: filter K+ out of the blodd with low K+ dialsate

Magnesium

• Intracellular cation: stored in muscle and bone

• helps to maintain normal

  • muscle and nerve funciton

  • cardiac rhythm

  • health immune system

  • bone strength

  • blood pressure

  • electrolyte (K+) and glucose levels (need Mg+ at normal range to help maintain K+)

Hypomagnesemia causes

• decreased intake: malnutrition, alcohol use

• decreased absorption: celiac disease, crohns disease

• Increased need in pregnancy

• Increased losses

  • GI losse: Laxatives, diarrhea

  • kidneys: increased urine, including with diuretics , drug induced

  • PPIs (proton pump inhibitor) > 1 year (chronic use)

  • aminoglucosides

  • amphotericin B

  • Cisplatin

Hypomagnesemia clinical manifestations

• less than 1.7

• neuromuscular manifestations

  • tremor, tetany, seizures

  • weakness

  • apathy

  • delirium

  • coma

• Cardiovascular

  • prolonged QTc

  • widening of QRS

  • Atrial and ventricular

  • atrial and ventricular dysrthythmias

• Hypokalemia

  • renal potassium wasting

• Abormalities of calcium metabolism

  • hypocalcemia

  • hypoparathyroidism

  • parathyoid hormone resistance

  • decreassed synthesis of calictrol

Hypomagnesemia treatment

• Oral or IV

• mylanta (a magnesium based antacid)

• magnesium sulfate tablets

• IV magnesium sulfate

  • 1-2 grams with life threatening conditions

Hypermagnesemia causes and treatment

• Impaired kidney function

  • dialysis

• Exogenous ingestion; excess Mylanta use

  • eliminate exogenous source magnesium

Hypermagnesemia clinical manifestations

• nausea and vomiting

• neurological impairment

  • confusion and lethargy

• Cardiovascular complications

  • hypotension and dysrhythmias

  • flushing

  • headache

Hypocalcemia Causes

• less than 8.6

• Decreased

  • decreased amount in diet

  • alcohol abuse

  • poor absorption

  • chronhs disease

  • hypoalbuminemia- calcium binds to albumin

  • increased loss

  • hypoparathyroidism (deficiency surgery/ neck)

  • renal failure

  • hyperphosphatemia

  • pancreatitis

  • laxatives and diarrhea

Hypocalcemia clinical manifestations

• Increased cell membrane excitability

• dysrhythmias

• increased bleeding tendencies

• anxiety, confusion, lethargy

• tremors, muscle spasms

• seizure

• decreased bone density

• Troussea sign

  • Use BP cuff to occlude blood flow

  • over 3 mins see carpal spams

• Chvostek sign

  • tap the facial nerve in front of the ear

  • elicit spasm or contraction: corner of mouth, nose, eye, and cheek muscles

Hypocalcemia treatment

• Oral replacement (mild):

  • calcium

  • vitamin D increases intestinal calcium absorption

• IV replacement (more severe)

  • calcium chloride- smaller dose and use central IV line

  • Calcium gluconate (peripheral IV)- less tissue necrosis with extravasation

• Calcium and phosphorus have inverse relationship

• Place in seizure precautions, tetany, muscle spasm

Hypercalcemia causes

• increased intake and reabsorption from bones

  • calcium antacids

  • calcium supplements

  • cancer

    • bone (shift of Ca from bone to ECF) , lung, breast, ovarian, prostate

  • immobilaztion

  • Vit D deficiency

  • Hypiphosphatemia

  • Decreased loss of calcoum

  • renal failure

  • thiazide diruetics

  • hyperparathyoidism

• Decreases neuromuscular excitability most common sign lethargy

Clinical Manifestations

• Dehydration: increase urine output

• Abdominal pain: cardiac dsyhrmias, neuro: fatigue, lethargy, confusion

Hypercalcemia treatment

• Treat underlying cause

• symptom management

• oral phosphate or calcitonin

• move calcium back into bone

• increased mobility (weight bearing)

• IVF and diuretic to increase excretion

Phosphorus

• 2.4-4.4

• mostly found in bones and blood

• inverse relationship with calcium

• key for: bone and tooth mineralization, cellular metabolism (essential for ATP formation O2 delivery function), acid-base balance, cell membrane, helping muscles contract and recover, using and storing energy

Hypophosphatemia

• less than 2.4

• Excess loss

• renal failure (especially acute)

• Hyperparathyroidism

• decreased intake: alcohol abuse

• cellular exchange in acid-base abnormality

• Clinical manifestations

  • usually realted to underlying causes

  • similar to those of hpyercacemia

    • fatigue, muscle weakness, bone pain, bone fractures

• Monitor LOC use seizure precautions monitor respiratory status

Hyperphosphatemia causes and clincal manifestations

• decreased excretion

• renal failure (especially chronic)

• hypoparathryoidism

• increased intke

• cellular exhange in acid base abnormailty

• Clinical manifestations

  • similar to hypocalcemia (and rarely alone)

  • muscle cramps

  • tetany

    • spasms of hands, feet, cramps overactive neuro reflexes

  • periorbital numbness or tingling

Hyperphosphatemia

• treat the underlying cause

• dialysis

• aluminum hydroxide and aluminum carbonate

• bind phosphorus and increase excretion

Chloride

• 96-106

• most abundant anion in blood and ECF important for electrical neutraluty in cells

• an extracellular ion

• maintains acid/base balance, works with Na to maintain somotic pressure/water balance

• balance with bicarbonate to help regulate acid base balance

Hyperchloremia

• dehydration, hypernatremia, diabetes insupidus, and large infusions of NaCl

• kidneys will secrete bicarbonate as compensatory mechanism with leads to hyperchloremic acidosis

• this can present as non-anion gap acidosis due to bicarb changes

Symptoms of Hyperchloremia

• muslce weakness, thist, weakness, faitgue, dehydration (very generalized)

Hyperchloremia treatment

• correct underlying cause

• for dehydration: rehydrate with PO or IV fluids

• investigationa nd treatment of diarrhea

• stop infusion of normal saline and correct with other IVF as appropriate

• note medications: azetazlamide, ASA overdosem thiasides

• Diabetic insipidus treatment and acute renal failure