Fluid and electrolytes

Isotonic solution

no net movement of water

ex: 0.9% NaCl and Lactated ringers

Hypotonic solution

fluid moves into cells

ex: 0.45% NaCl

Hypertonic solution

fluid leaves cells

ex: 3% NaCl

Fluid volume deficit

loss of both water and electrolytes from the extracellular fluid; also called hypovolemia

Dehydration

loss of pure water from the body

Causes of extracellular volume deficit

-Abnormal loss of body fluids (diarrhea, vomiting, hemorrhage, polyuria)

-Inadequate fluid intake

-Plasma to interstitial fluid shift (burns)

extracellular volume deficit symptoms

-Lethargy, confusion, weakness and dizziness

-Thirst, dry mucous membranes, cold skin, tenting, decreased cap refill

-Postural hypotension

-Increased HR, increased RR

-Low urine output, concentrated urine,

-Weight loss, seizures, coma

Fluid volume excess causes

-Excess intake of fluids

-Abnormal retention of fluid (heart or renal failure)

-Interstitial-to-plasma fluid shift (burn patients after 48-72 hours)

Fluid volume excess symptoms

-Weight gain

-Headache, confusion, lethargy

-Edema, JVD, S3, bounding pulse

-Increased blood pressure

-Polyuria

-Dyspnea, crackles, pulmonary edema

-Muscle spasms

Phosphorus lab value

3-4.5 mg/dL

Sodium lab value

136-145 mEq/L

potassium lab value

3.5-5.0 mEq/L

calcium lab value

9.0-10.5 mg/dL

magnesium lab value

1.3-2.1 mEq/L

Sodium functions

ECF volume and concentration

Nerve impulses

Muscle contractility

Acid-base balance

Hypernatremia causes

Inadequate water intake (unconscious or cognitively impaired)

Excess water loss (diarrhea or high fever)

Decreased ECF volume hypernatremia S/S

Restless, agitation, lethargy, seizures, coma

Intense thirst, dry swollen tongue, dry mucous membranes

Postural hypotension, decreased CVP, weight loss, increased pulse

Weakness and muscle cramps

Normal/increased ECF volume hypernatremia S/S

Restlessness, agitation, twitching, seizures, coma

Intense thirst, flushed skin

Weight gain, edema

Increased blood pressure, increased CVP

Decreased ECF volume hypernatremia treatment

Fluid replacement (PO or IV with isotonic)

Normal/increased ECF volume hypernatremia treatment

Dilute the high sodium using sodium free IV solutions (D5W)

Promote sodium excretion with diuretics

Dietary sodium restriction

Seizure precautions

Hyponatremia causes

Loss of sodium-containing fluids or water excess or both

ECF hypoosmolality causes fluid to move into cell and swell them

-Diuretics, vomiting, diarrhea, inadequate salt intake, hypertonic IV solutions, GI suctioning

Hyponatremia S/S

mild- headache, irritability, difficulty concentrating

severe- confusion, vomiting, seizures, coma

Loss of sodium and fluid hyponatremia treatment

Isotonic IV solutions

Oral fluid intake

Stop diuretics

Dilutional hyponatremia treatment

Fluid restriction

Diuretics

Demeclocycline

Potassium functions

Resting membrane potential in nerve and muscle cells

Cellular growth

Maintaining normal cardiac rhythm

Acid-base balance

Concentration of K+ inversely related to Na+

Hyperkalemia causes

Massive intake of K+ (salt substitutes)

Impaired renal excretion (primary cause)'

Shift from ICF to ECF from acidosis (H+ shift into cell and K+ shift out to balance out)

Medications: digoxin, beta-blockers, ace inhibitors, potassium sparing diuretics

Hyperkalemia S/S

Dysrhythmias (tall peaked T wave)

Fatigue, confusion

Tetany, muscle cramps

Weak or paralyzed skeletal muscles

Abdominal cramping, vomiting, or diarrhea

Hyperkalemia treatment

Stop K+ intake

Increase K+ excretion (diuretics, kayexalate, dialysis)

Force movement of K+ from ECF to ICF using dextrose and insulin, sodium bicarb or beta 2 agonist (albuterol)

Stabilize cardiac membranes using IV calcium

Hypokalemia causes

GI losses (diarrhea and vomiting)

Renal losses (magnesium deficiency, diuretics)

Metabolic alkalosis or insulin administration (shifts K+ into ICF)

Decreased dietary K+ intake

Hypokalemia S/S

Muscle weakness (including respiratory and skeletal muscles)

ECG changes (prominent U wave, ST depression)

Nausea, vomiting, decreased GI motility

Hyperglycemia

Hypokalemia treatment

Administration of potassium (oral is preferred or IV)

Increased dietary K+ intake (bananas, potatoes, tomatoes)

Calcium functions

Formation of teeth and bone

Blood clotting

50% bound to albumin

Transmission of nerve impulses

Myocardial contractions

Muscle contractions

Regulated by parathyroid hormone and calcitonin

Requires activated vitamin D for absorption

Hypercalcemia causes

Hyperparathyroidism (two thirds of cases)

Cancer (esp. bone cancer)

Vitamin D overdose (rare)

Prolonged immobilization (bones break down and release Ca into blood)

Hypercalcemia S/S

Fatigue, lethargy, weakness, confusion

Decreased reflexes

Hallucinations, seizures, coma

Hypertension, dysrhythmias

Bone pain, fractures

Polyuria, dehydration

(BACKME)

Mild hypercalcemia treatment

Stop medications that may be contributing

Diet low in calcium

Weight bearing activity (stops bone breakdown)

Hydration

Severe hypercalcemia treatment

IV isotonic saline

Calcitonin (inhibits movement of calcium into plasma)

Biphosphonates (inhibit osteoclast activity)

Dialysis (in life-threatening situations)

Hypocalcemia causes

Decreased production of PTH

Multiple blood transfusions (6-10 transfusions in 24 hours)

Alkalosis

Increased calcium loss

Hypocalcemia S/S

Trousseau's sign

Chvosteck's sign

seizures

tetany

Dysrhythmias

CNS changes

numbness

tingling

Hypocalcemia treatment

Treat underlying cause

Increase dietary calcium

Vitamin D

IV calcium gluconate

Change loop diuretic to thiazide

Phosphorus functions

Majority in bones and teeth

Function of muscle, red blood cells, and nervous system

Acid-base buffering system in kidneys

ATP production

Cellular uptake of glucose

Metabolism of carbs, proteins, and fats

Regulated by PTH

Inversely related to calcium

Hyperphosphatemia causes

Renal failure

Excess intake of phosphate (often from enemas/laxatives)

Excess intake of vitamin D

Hypoparathyroidism

Hyperphosphatemia S/S

Tetany, muscle cramps, paresthesia, hypotension, dysrhythmias, seizures (hypocalcemia)

Calcified deposition in soft tissue

Hyperphosphatemia treatment

Treat underlying cause

Restrict dietary intake of phosphate

Oral phosphate binding agents (calcium carbonate AKA Tums)

Volume expansion and forced diuresis with loop diuretic

Dialysis

Hypophosphatemia causes

Malnourishment/malabsorption

Alcohol withdrawal

Diarrhea

Phosphate-binding antacids

Inadequate replacement during parenteral nutrition

Hypophosphatemia S/S

CNS depression

Muscle weakness and pain

Respiratory and heart failure

Rickets, osteomalacia, rhabdomyolysis

Hypophosphatemia treatment

Increase oral intake - Dairy

Supplementation (can be irritating to GI tract)

IV supplementation with potassium phosphate or sodium phosphate

Magnesium functions

DNA and protein synthesis

Blood glucose control

BP regulation (low mag = high BP)

ATP production/use with Na+/K+ pump

Controlled by kidneys and GI tract

Hypermagnesemia causes

Increased intake of products when renal insufficiency or failure is present; maalox and milk of magnesia

Excess IV magnesium admin

Hypermagnesemia S/S

Hypotension, facial flushing

Impaired DTRs

Muscle paralysis

Respiratory and cardiac arrest

Hypermagnesemia treatment

Avoid Mg containing food or drugs

Fluid admin in patients with normal renal function to promote excretion

Calcium gluconate IV to counteract effects

Dialysis of renally impaired

Hypomagnesemia causes

Prolonged fasting or starvation

Chronic alcoholism

Fluid loss from gastrointestinal tract

Prolonged parenteral nutrition without supplementation

Diuretics

Hyperglycemic osmotic diuresis

Hypomagnesemia S/S

Resembles hypocalcemia: muscle cramps, tremors, hyperactive DTRs, chvostek's and trousseau's sign, confusion, vertigo, seizures

Dysrhythmias

Hypomagnesemia treatment

Treat underlying cause

Oral or IV supplementation (monitor closely for hypotension and arrhythmias with IV)