Fluids & Electrolytes

Acids & Bases

Distribution of Body Fluids
Blood is a mixture of particles
 OSMOSIS
Water Movement Between Fluid Compartments

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 Osmolality

It is the concentration of a solution

expressed as
the total number of solute particles
per kilogram of solution.
 OSMOTIC FORCES
Water Movement Between Fluid Compartments
Osmolality is a ratio of water to solutes (particles in solution).

HYPO-osmolality: HYPER-osmolality: ISO-osmolality:

Too much water Too many solutes Equal ratio of solutes
outside the cell; outside the cell; inside and outside the
water flows INTO water flows OUT of cell; water stays put
the cell until it explodes the cell until it shrinks up

The ratio: WATER:particles water:PARTICLES water:particles

Total body fluid alterations can be isotonic, hypotonic, or hypertonic.

 AQUAPORINS
Water Movement Between Fluid Compartments
Aquaporins (or water channels) are channel proteins that form pores in the cell membrane
to facilitate water transport between cells.

Aquaporins are regulated by Antidiuretic Hormone (ADH).

 These two forces are called
STARLING FORCES.

Water pressure Proteins attract water

PUSH PULL

Example: When a client has

Analogy: Water pushes into a malnutrition and their serum
basement when there is flooding albumin (protein) is low, water is
and the water table beneath the attracted to the interstitial spaces
house has risen. (spaces between cells outside of
the blood vessels) and EDEMA is
the result.
Chem Review
 2 Basic Types of Body Fluids
Colloid: Albumin Crystalloid: salt in water
 noncrystalline substance consisting of
large molecules of
 one substance (like albumin)
 dispersed through a second substance (like
water).

 Easily forms crystals when frozen.

 A water-based fluid that is a solution of
 mineral salts
 other small, water-soluble molecules. (ie: sodium
chloride)

• Water is attracted to albumin and will cross

through membranes to get to it.
• 1 gram of albumin can hold ~20 mL of water.
 STARLING FORCES
Water Movement Between Fluid Compartments

A. Filtration Net Filtration B. Reabsorption

Interstitial

Capillary

A. Forces favoring Filtration: when fluid/particles leave the capillary

 Higher Plasma (capillary) hydrostatic pressure (pushing water out)
 Higher Interstitial oncotic pressure (pulling water into the interstitial space)

B. Forces favoring Reabsorption: fluid/particles return to the capillary

 Higher Plasma (capillary) oncotic pressure (pulling water into the capillary)
 Higher Interstitial hydrostatic pressure (pushing water out)
 Edema
 Accumulation of fluid within the interstitial
spaces
 Causes:
 Increase in capillary hydrostatic pressure
 Decrease in plasma oncotic pressure
 Increase in capillary permeability
 Lymph obstruction (lymphedema)
 Localized vs. generalized
 Pitting edema
 Chem Review
The atoms in an ionic molecule DO NOT share electrons. (i.e.: table salt)
Atoms in a covalent molecule DO share electrons and be polar (i.e.: water) or nonpolar (i.e.: oxygen).

An ion is an atom or molecule with a net electric charge due to

the loss or gain of one or more electrons.

Cation or a Anion or a
“Cat-ion” is a “An-ion” is a
positively negatively
charged ion. charged ion.
 Sodium and Chloride Balance

 Sodium
 Primary ECF cation (positive ion)
 Regulates osmotic forces, thus water
 Roles:
• Neuromuscular irritability
• acid-base balance
• cellular chemical reactions and membrane transport
 Chloride
 Primary ECF anion (negative ion)
 Provides electroneutrality
Renin-angiotensin-aldosterone system (RAAS System & NaCl Balance)
 Aldosterone—leads to sodium and water reabsorption back into the circulation and excretion of potassium
 Natriuretic peptides (natrium = sodium; -uretic = diuresis): causes sodium and water excretion
 How the body balances water

 Thirst perception
 Osmolality receptors: Hyperosmolality and plasma
volume depletion
• Volume receptors (blood volume)
• Baroreceptors (blood pressure)
 Anti-diuretic hormone (ADH) secretion
 Reduces urine production (diuresis)
 Increases water reabsorption into the plasma
 Antidiuretic Hormone (ADH) System
Increased attraction of
water to the vasculature
BP drop

Antidiuretic hormone

Reduced attraction of
water to the vasculature BP Increase
 Sodium (Na)
135 to 145 mEq/L
Hyponatremia
Hypernatremia
 Serum sodium level <135 mEq/L
 Serum sodium >145 mEq/L
 Sodium deficits cause plasma hypo-
 Related to sodium gain or water
osmolality and cellular swelling
loss
 Causes:
 Water movement from the ICF
 Pure sodium loss
 Low intake
to the ECF
 Dilutional hyponatremia
• Intracellular dehydration
 Manifestations
 Manifestations:
 Decreased osmolality • Clinical
 Thirst, weight gain, bounding
 Hyponatremia decreases the ECF osmotic
pressure, and water moves into the cell via pulse, and increased blood
osmosis pressure
 Cells expand • Central nervous system
 Most life-threatening: cerebral edema and  Muscle twitching and
increased intracranial pressure hyperreflexia (hyperactive
 Lethargy, confusion, decreased reflexes, seizures, reflexes), confusion, coma,
and coma convulsions, and cerebral
 With loss of ECF and hypovolemia: hypotension, hemorrhage
tachycardia, decreased urine output
 If dilutional from excess water: weight gain,
edema, ascites, jugular vein distention
 Potassium (K+)
 Major intracellular cation
 Concentration maintained by Na+/K+ pump
 Regulates intracellular electrical neutrality in relation to Na+ and H+
 Essential for transmission and conduction of nerve impulses, normal
cardiac rhythms, and skeletal and smooth muscle contraction
 Changes in pH affect K+ balance
 Hydrogen ions accumulate in the ICF during states of acidosis; K+
shifts out to maintain a balance of cations across the membrane;
result is hyperkalemia
 Aldosterone, insulin, and epinephrine influence serum K levels
 Kidney is most efficient regulator
 Potassium adaptation: Slow changes tolerated better than acute
 Potassium (K)
3.5 to 5.0 mEq/L

Hypokalemia Hyperkalemia
 K level <3.5 mEq/L  K level >5.0 mEq/L
 Causes  Hyperkalemia is rare
 reduced intake of K because of efficient renal
 increased entry of K into excretion
cells  Caused by increased
 increased loss of K in the intake, shift of K+ from ICF
kidneys
into ECF, decreased renal
 Manifestations (depend on excretion, insulin deficiency,
rate and severity) or cell trauma
 Membrane  Mild attacks: Increased
hyperpolarization causes a
neuromuscular irritability
decrease in neuromuscular
excitability, skeletal muscle  Restlessness, intestinal
weakness, smooth muscle cramping, and diarrhea
atony, and cardiac  Severe attacks: Decreases
dysrhythmias the resting membrane potential
 Muscle weakness, loss of
muscle tone, and paralysis
 Cardiac dysrhythmias
 Calcium and Phosphate
 Calcium and phosphate concentrations are
rigidly controlled by parathyroid hormone
(PTH), vitamin D, and calcitonin
 Calcium
Normal: Serum concentration 8.8 to 10.5 mg/dl

 99% of calcium is located in the bone as

hydroxyapatite
 Necessary for structure of bones and teeth,
blood clotting, hormone secretion, cell
receptor function, plasma membrane stability,
transmission of nerve impulses, muscle
contraction
 Calcium
Hypocalcemia Hypercalcemia
 Causes:  Causes:
 Inadequate intestinal absorption,  Hyperparathyroidism
deposition of ionized calcium into  Bone metastases with calcium
bone or soft tissue, blood resorption from breast, prostate,
administration renal, and cervical cancer
 Decreases in PTH and vitamin D  Sarcoidosis
 Nutritional deficiencies occur with
 Excess vitamin D
inadequate sources of dairy
 Many tumors that produce PTH
products or green, leafy vegetables
 Effects:
 Effects:
 Increased neuromuscular
 Many nonspecific: fatigue,
excitability weakness, lethargy, anorexia,
• Tingling, muscle spasm (particularly nausea, constipation
in hands, feet, and facial muscles),  Impaired renal function, kidney
intestinal cramping, hyperactive stones
bowel sounds  Dysrhythmias, bradycardia,
 Severe cases: convulsions & cardiac arrest
tetany, laryngeal spasm  Bone pain, osteoporosis
 Prolonged QT interval, cardiac
arrest
 Phosphate
Normal: Serum concentration 2.5-5.0 mg/dl

 Like calcium, most phosphate is also located

in the bone
 Provides energy for muscle contraction
 Parathyroid hormone, vitamin D3, and
calcitonin act together to control phosphate
absorption and excretion
 Phosphate
Hypophosphatemia Hyperphosphatemia
 Causes:
 Causes:
 Intestinal malabsorption (vitamin D  Acute or chronic renal failure with
deficiency, use of magnesium- and significant loss of glomerular filtration
aluminum-containing antacids, long-  Treatment of metastatic tumors with
term alcohol abuse) chemotherapy that releases large amounts
 Malabsorption syndromes of phosphate into serum
 Respiratory alkalosis  Long-term use of laxatives or enemas
containing phosphates
 Increased renal excretion of phosphate
associated with hyperparathyroidism  Hypoparathyroidism
 Effects:
 Effects:
 Reduced capacity for oxygen transport  Symptoms primarily related to low serum
by red blood cells, thus disturbed calcium levels (caused by high phosphate
energy metabolism levels) similar to the results of
 Leukocyte and platelet dysfunction hypocalcemia
 Deranged nerve and muscle function  When prolonged, calcification of soft
 In severe cases, irritability, confusion, tissues in lungs, kidneys, joints
numbness, coma, convulsions,
possibly respiratory failure,
cardiomyopathies, bone resorption
 Magnesium
Normal: Serum concentration 1.5 to 2.5 mEq/L

 Intracellular cation
 Acts as a cofactor in intracellular enzymatic
reactions
 Increases neuromuscular excitability
 Magnesium
Hypomagnesemia Hypermagnesemia
 Causes:  Causes:
 Malnutrition  Usually renal insufficiency or
 Malabsorption syndromes failure
 Excessive intake of magnesium-
 Alcoholism
containing antacids
 Urinary losses (renal tubular
 Adrenal insufficiency
dysfunction, loop diuretics)
 Effects:
 Effects:
 Skeletal smooth muscle
 Behavioral changes
contraction
 Irritability  Excess nerve function
 Increased reflexes  Loss of deep tendon reflexes
 Muscle cramps  Nausea and vomiting
 Ataxia  Muscle weakness
 Nystagmus  Hypotension
 Tetany  Bradycardia
 Convulsions  Respiratory distress
 Tachycardia
 Hypotension
 Acid-Base Balance

 Acid-base balance is carefully regulated

to maintain a normal pH via multiple
mechanisms
 Buffering Systems

 A Buffer is a solution that contains an acid and a

base, or a salt, that maintains a constant hydrogen
ion concentration (pH).
 A buffer is a chemical that can bind excessive
H+ or OH– without a significant change in pH
 The most important plasma-buffering systems
are the carbonic acid–bicarbonate pair
 pH
 Normal pH is 7.35-7.45
 H+ must be neutralized or excreted
 The bones, lungs, and kidneys are the major organs involved in the
regulation of acid-base balance
 Body acids exist in two forms:
 Volatile: H2CO3 (can be eliminated as CO2 gas)
 Nonvolatile: Eliminated by the renal tubules with the regulation of HCO 3–

LUNGS KIDNEYS
 Acidosis & Alkalosis

 4 categories of acid-base imbalances:

 Respiratory acidosis
• ↑ pCO2 as a result of ↓ ventilation
 Respiratory alkalosis
• ↓ pCO2 as a result of XS ventilation
 Metabolic acidosis
• ↓ HCO3– or ↑ in noncarbonic acids
 Metabolic alkalosis
• ↑ HCO3– usually caused by an XS loss of metabolic acids

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