4. 4
• Fluid compartments are separated by
membranes that are freely permeable to water.
• Movement of fluids due to:
– Diffusion
– Osmotic pressure
– Active transport
– Hydrostatic pressure
– Reabsorption
Movement of Fluids
11. 11
TONICITY:
Isotonic – A solution that
has the same solute
concentration as another
solution to which it’s
being compared
• i.e. sodium in blood vs.
0.9% NSS
12. 12
• Hypertonic - A
solution that has a
higher solute
concentration than
another solution to
which it’s being
compared
• Dextrose 5% in
NSS
TONICITY:
13. 13
• Hypotonic - A
solution that has a
lower solute
concentration than
another solution to
which it’s being
compared
• 0.45%NSS
TONICITY:
14. 14
Balance
Fluid and electrolyte homeostasis is maintained in the body
• Neutral balance: input = output
• Positive balance: input > output
• Negative balance: input < output
15. Fluid Gain & Loss
Routes of Gain and Loss:
Kidneys (urine)
Skin (perspiration)
Lungs (respiration)
GI Tract (feces)
16. Fluid Gain & Loss
Average Intake of Body H2O
= 2600 ml/day
Liquid = 1500 ml
Solid Foods = 800 ml
Oxidation = 300 ml
17. Fluid Gain & Loss
Sensible Loss
• Fluid loss that can be measured
– Urination
– Defecation
– Bleeding
– Wound drainage
– Gastric drainage
– Vomiting
18. Fluid Gain & Loss
Insensible Loss
• Fluid loss that cannot be measured
– Perspiration
– Respiration
– Changes in humidity levels, respiratory rate
and depth, and fever affect insensible loss
19. Fluid Gain & Loss
Average Output of Body H2O
= 2600 ml/day
Urine = 1500 ml
Feces = 100 ml
Lungs = 400 ml
Skin = 600 ml
20. Balancing Systems
Renal System (kidneys)
–RF = difficulty maintaining fluid balance
–Na+ & K+ are either filtered or
reabsorbed via the renal system
21. Balancing Systems
Antidiuretic Hormone (ADH)
–Water-retaining hormone
–Hypothalamus senses low blood volume
& increased serum osmolality; triggers
its release from the pituitary gland
–Prompts kidneys to retain H2O
–Increases concentration of urine
22. Balancing Systems
Renin-Angiotensin-Aldoseterone
System (RAAS)
–Release of renin triggered by low
pressures
–Angiotensin II potent vasoconstrictor
and triggers the release of aldosterone
from the adrenal cortex
–Aldosterone = fluid retention and
secretion of K+; triggers the thirst center
23. Balancing Systems
Atrial Natriuretic Peptide (ANP)
– Released when atrial pressures increase
– Opposes the RAAS (shuts it off)
– Key Functions of ANP:
• Suppresses serum renin levels
• Decreases aldosterone release
• Increases glomerular filtration rate (excretion of
Na+ and H2O)
• Decreases ADH release
• Decreases vascular resistance by causing
vasodilation
24. Balancing Systems
Thirst Mechanism
– Simplest mechanism in maintaining fluid
balance
– Increases after even small fluid loss
– Increase in salty foods dries mucous
membranes, which stimulates the thirst center
in the hypothalamus
25. Hypovolemia
blood volume caused by internal/external bleeding,
fluid losses, or inadequate fluid intake.
(AKA: Fluid Volume Deficit (FVD) or Extracellular Fluid Volume Deficit (ECFVD))
26. Hypovolemia
FVD occurs when loss of ECF exceeds intake of fluid.
Hypovolemia or FVD ≠ dehydration
Dehydration is loss of H2O only!!
FVD → Fluid Loss = Electrolyte Loss
Ratio Remains the Same (usually)
28. Hypovolemia
Treatment:
Infusion of Isotonic IV solutions: Hypotensive patients
Infusion of Hypotonic IV solutions: Normotensive patients
Hypovolemia d/t blood loss: Blood transfusion
29. Hypervolemia
ECF → H2O gain is balanced 𝒄 retention of sodium.
• Usually 2 retention of Na+
• Concentration of sodium to H2O is balanced.
• serum sodium levels WNL (usually)
(A.K.A. Extracellular Fluid Volume Excess (ECFVE))
30. Hypervolemia
Hormonal Imbalances - ADH
• Can occur 2 heart failure, renal failure, or cirrhosis.
• Fluid overload r/t administration of excessive IV fluids
• Dietary: Excessive sodium intake
34. Sodium
• Accounts for 90% of ECF cations.
• Almost all Na+ is found in ECF; 10% in ICF.
• Na+ attracts fluid + helps preserve ECF volume/fluid
distribution.
• Na+ helps transmit impulses in nerve/muscle fibers, &
combines w/ Cl- & HCO3 to regulate acid-base balance
35. Sodium
• Excreted mainly via the kidneys (GU)
– Also via the GI tract and perspiration
• Increased Na+ levels trigger thirst & ADH
• Sodium-Potassium pump helps maintain normal Na+
levels
– Pump also creates an electrical charge for both cardiac &
neuromuscular function
40. Hyponatremia
Treatment:
• Administration of oral or IV Na+ (3%) Supplements
• Encourage foods high in Na+
• Fluid restriction
• Monitor Neuro Status
• Monitor for Arrhythmias
• Normovolemic hyponatremia
– Vaprisol (conivaptan) – IV infusion
– Samsca (tolvaptan) - PO
41. Hypernatremia
Causes:
• Dehydration/Hypovolemia
• Diabetes Insipidus
• Ingestion of Hypertonic Solutions
• IV Infusion of Hypertonic Solutions
• Cushing’s Syndrome
• Hyperaldosteronism
• Loss of pure water (excessive sweating or respiratory infections)
45. Potassium
Potassium is gained by intake and lost by excretion.
If either is altered, hyperkalemia or hypokalemia may result!
Regulated by aldosterone and insulin
46. Potassium
Potassium levels directly affect cell, nerve, & muscle
function:
– Maintains electrical neutrality and osmolality of cells
– Aids in neuromuscular transmission of nerve impulses
– Assists skeletal & cardiac muscle contraction and electrical
conductivity
– Affects acid-base balance in relationship to H+ (another cation)
50. Hypokalemia
May be a result of acid-base imbalances = alkalosis
• In alkalosis, K+ moves into cell to maintain balance,
-may lead to hypokalemia
51.
52. Treatment
• Oral or IV Potassium Chloride
Replacement
• D/C or adjust medications that may
cause hypokalemia
• Reverse alkalosis, if cause
• Monitor closely for arrhythmias
• Monitor Respiratory Status
• Monitor LOC
• Monitor GI symptoms
55. Hyperkalemia
May be a result of acid-base imbalances = acidosis
In acidosis, excess [H+] move into cells & push K+ into ECF,
- may lead to hyperkalemia as K+ moves out of cell to maintain
balance.
56.
57. Hyperkalemia
Treatment:
Medications:
– Cation-exchange resins (bind with K+ and excreted via feces)
– IVP insulin & glucose (K+ binds to insulin)
– IV Ca++ (protect the heart from the effects of hyperkalemia)
– Sodium bicarbonate (to reverse acidosis)
– Diuretics (non-K+ sparing)
– Beta2 Adrenergic agonists (epinephrine, albuterol)
D/C meds that may cause hyperkalemia
Restrict foods with K+
Dialysis for renal failure
Monitor closely for arrhythmias
Monitor Blood Pressure
Monitor GI symptoms
59. Calcium
• 99% Ca++ in bones; 1% in serum/soft tissue (measured in
blood serum levels)
• Found in both ECF & ICF
• Can be measured in 2 ways:
– Total serum calcium (total Ca++in blood)
– Ionized calcium level (various forms of Ca++ in ECF)
• 41% ECF Ca++ is bound to protein; 9% bound to citrate or
other organic ions
60. Calcium
• Ca++ functions in the following ways:
– Responsible for formation of teeth & bones
– Helps maintain cell structure & function
– Plays a role in cell membrane permeability & impulse
transmission
– Affects contraction of cardiac, smooth, and skeletal muscle
– Participates in blood-clotting process
61. Calcium
Ca++ helps K+ & Na+ move into and out
of cells in the sodium-potassium
pump mechanism
62. Hypocalcemia
Causes:
• Vitamin D Deficiency
– Vitamin D promotes Ca++ absorption in intestines, resorption from bones,
and kidney resorption all of which raise Ca++ levels
• Deficiency of parathyroid hormone
– Calcitonin, secreted by PTH, helps regulate Ca++
– s absorption of Ca++/enhances excretion by kidneys
• Inefficient parathyroid hormone
64. Hypocalcemia
Management…
• PO or IV calcium replacement
(depends on severity of symptoms or deficiency)
• Vitamin D supplement
• Encourage foods high in calcium
76. Hypomagnesemia
• Does not produce specific EKG changes
• May contribute to arrhythmias caused by digoxin toxicity,
ischemia, or K+ imbalances
• Monitor:
– EKG for Arrhythmias
– Muscle cramps
77. Hypomagnesemia
Replacement of Mg: PO or IV
• PO = Mg Oxide 400mg tabs
• MgSo4 IV administration is usually given at a rate of 1 gram/hr
(1 gram/100 ml)
• Encourage foods high in magnesium