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intracellular fluid
fluid in cells
2/3 of body water
extracellular fluid
interstitial
intravascular
plasma/serum
transcellular fluid
CSF
fluid in peritoneal, pericardial, & pleural spaces
fluid in joint spaces
body fluid transport
helps transport gases, nutrition, and waste
generates electrical activity
food → energy
cell membrane
O2 and CO2 pass directly through
Ions need transport mechanisms (or can be exchanged if they have the same charge)
water uses osmosis
diffusion
movement of charged or uncharged particles along a concentration gradien
osmosis
movement of water across a semipermeable membrane
primary solute in body
sodium
primary solvent in body
water
what does the distribution of fluids between ICF and ECF rely on
concentration of ECF sodium and water content
low osmolarity
less than 275
low amounts of solutes → dilute
elevated osmolarity
greater than 295
large amounts of solutes → concentrated
changes in sodium are usually present by proportionate changes in
water volume
tonicity
effective osmolarity of a solution
osmoreceptors: water & Na regulation
sensory neurons located in/near hypothalamus
shrink/swell based on osmolarity
increase thirst response & increase ADH release when stimulated
baroreceptors stimulate
sympathetic response
ADH release
sympathetic response water & Na regulation
dec GFR, slows Na filtration from blood
stimulates kidneys to release renin
ADH water & Na regulation
tells kidneys to hold onto H2O at renal tubules → inc volume
heart: water & Na regulation
ANP released in response to atrial stretch & overfilling
BNP stimulates kidneys to rid body of Na
renin: water & Na regulation
released from either SNS stimulation or dec in blood flow to organ occurs
aldosterone promotes Na & H2O absorption in kidneys
isotonic fluid volume deficit
dec in ECF with equal losses of H2O & sodium
causes of isotonic fluid volume deficit
GI = vomiting, diarrhea, NG tubes, fistulas
urine = diuretics, hyperglycemia
skin = sweating (fever/exercise)
endocrine = low aldosterone → Na lost in urine
transcellular fluid accumulation
symptoms of isotonic fluid volume deficit
weight loss
inc thirst
dec urine output
dec skin & tissue turgor
dry mucous membranes
sunken eyeballs
depressed fontanels in infants
postural hypotension
weak, rapid pulse
dec capillary refill
severe - hypovolemic shock
isotonic volume overload
isotonic expansion of ECF compartment
inc interstitial & vascular volumes
when does isotonic volume overload occur
Na excess with proportionate inc in H2O
circulatory overload
causes of isotonic volume overload
heart failure
renal failure
liver failure
corticosteroid excess
symptoms of isotonic volume overload
weight gain
edema
bounding pulses
venous distension
pulmonary edema
causes of edema
inc capillary filtration/hydrostatic pressure
dec capillary oncotic pressure
inc capillary permeability
lymph obstruction
causes of inc capillary filtration/hydrostatic pressure
inc arterial pressure
dependent edema
inc resistance to outflow - venous obstruction
thrombophlebitis
capillary distension
inc vascular volume (CHF, kidney disease)
what does capillary hydrostatic pressure do
pushes water out of capillary into interstitial spaces
capillary distension symptoms
edema
excessive Na and water retention
dyspnea
crackles
SOB
non-productive cough
what causes dec capillary oncotic pressure
inadequate production or loss of proteins (albumin)
liver failure, malnutrition, extensive burns
what does capillary oncotic pressure do
pulls water back into capillary
what type of edema is caused by dec capillary oncotic pressure
generalized edema
what type of edema is caused by inc capillary filtration/hydrostatic pressure
dependent edema
what happens when cap permeability is inc?
cap pores enlarge → proteins leak interstitially
what causes inc cap permeability
allergic reactions
inflammation
burns
lymphedema
edema due to impaired lymphatic flow
honeycomb appearance
what does impaired lymph flow lead to
lymphedema
causes of lymphedema
cancer
lymph node removal
trauma
infection
edema
palpable swelling from inc interstitial fluid volume
types of peripheral edema
pitting
non-pitting
pitting edema
accumulation of interstitial fluid exceeding absorbing capacity of surrounding tissue
non-pitting edema
condition in which plasma proteins have accumulated in the tissue spaces & coagulated
what does non-pitting edema look like
firm & discolored
transcellular edema (third spacing)
trapping of ECF into transcellular compartments and serous cavities
types of transcellular edema
ascites
pleural effusuion
pericardial effusion
what is the major cation of ECF
sodium (Na+)
what regulates sodium levels
kidneys
aldosterone
natriuretic peptides
when is aldosterone secreted
depressed Na levels
inc K levels
dec renal perfusion
what do natriuretic peptides do
inc Na and water excretion
sodium is necessary for which body functions
osmotic transfer
acid base balances
neuromuscular and muscular excitability
depolarization of cell membranes of excitable cells
hyponatremia
low blood sodium levels
hypotonic hyponatremia
dilution
excessive sweating, GI losses, SIADH, HF
hypertonic hyponatremia
sodium in the ECF becomes diluted as water moves out of body cells in response to the osmotic effects of the elevated blood glucose level.
osmotic shift from ICF to ECF
hyperglycemia
hyponatremia manifestations
alters ability of cells to normally depolarize/repolarize
muscle cramps/motor weakness
weakness/fatigue
headache, lethargy, confusion
seizures
rapid correction of sodium can cause
osmotic demyelination syndrome = destruction of myelin sheath of axons passing through brain stem
hypernatriemia
high sodium blood levels
causes of hypernatriemia
disproportionate loss of body water in relation to Na
through urine, GI tract, lungs
H20 not replaces
Na gain
hypernatriemia manifestations
thirst
low urine output
inc urine osmolarity
weak, thready, elevated pulse
dec BP
dry mucus membranes, rough tongue, trouble swallowing
irritability, restlessness, dec reflexes, headache
seizures & coma can occur
what does K do
maintains intracellular osmolartity
maintains acid-base balance
catalyst to transform CHOs into energy
converts glucose into glycogen
convert amino acids into proteisns
critical in conduction of nerve impulses and muscle excitability
regulation of K
renal
aldosterone (lowers levels)
K/H exchange mechanism
transcellular buffer system - redistributes btwn ECF & ICF
removes K+ from or releases K into serum as needed
K temporarily shifted into RBCs, muscle, liver & bone
what happens to the resting potential when K levels are low
it moves away from the threshold → takes a greater stimulus to reach threshold potential & open up sodium channels
hypokalemia
low K blood levels
causes of hypokalemia
inadequate intake
fad diets, ED, elderly
excessive loss
diuretic therapy, metabolic acidosis, excessive GI loss from vomiting/diarrhea
hypokalemia manifestations
neuro
weakness
fatigue
paresthesia
CV
ECG changes
arrythmias
delayed ventricular depolarization & freq of action potentials
GI
nausea/vomiting
distension
GU
polyuria
what happens to the resting potential when K levels are high
resting potientia; moves toward threshold → cells fire more easily → cannot depolarize
hyperkalemia
high K blood levels
causes of hyperkalemia
dec renal elimination
CRF, ARF
depressed aldosterone
movement of K from ICF to ECF
acidosis, tissue injury
excessive rapid rate of administration
mild hyperkalemia symptoms
restlessness
intestinal cramping
diarrhea
ECG changes, peaked T waves
weakness
paresthesia
severe hyperkalemia symptoms
muscle weakness
loss of muscle tone
possible paralysis
lethal arrhythmias (vfib)
cardiac arrest
severe bradycardia
what hormone helps to maintain calcium concs in ECF
PTH
PTH functions
tells kidneys to get rid of phosphorus and keep calcium
inc renal activation of vitamin D → acts on intestines to absorb more Ca during digestion
hypoparathyroidism
deficient PTH secretion
causes of hypoparathyroidism
congenital
autoimmune
surgery
hypomagnesemia
what does hypoparathyroidism result in
low serum ionized Ca
low serum calcium
symptoms of hypoparathyroidism
neuro = paresthesia, muscle spasms, tetany, hyperactive reflexes
CV = hypotensison, HF, long QT, arrhythmias
skeletal = fractures
hyperparathyroidism
inc PTH secretion
types of hyperparathyroidism
primary
hyperplasia
adenoma/cancer of gland
secondary
chronic renal failure
chronic malabsorption of Ca
hyperparathyroidism results in
high Ca levels
renal osteodystrophy
symptoms of hyperparathyroidism
hypocalcemia
low blood Ca levels
causes of hypocalcemia
nutritional deficiencies
lack of vitamin D
renaal failure
hypoparathyroidism
alkalosis
hypocalcemia manifestations
neuro = paresthesia, muscle spasms, tetany, hyperactive reflexes
CV = hypotensison, HF, long QT, arrhythmias
skeletal = fractures
assessment of hypocalcemia
Chvostek – tapping facial nerve – spasm of lip, nose, face.
Trousseau – BP cuff inflated 10mmHg above SBP for 3 minutes
See contraction of hand and fingers
hypercalcemia
high Ca levels
causes of hypercalcemia
malignancy
cancer destroys bone → Ca released
tumors produce PTH
hyperparathyroidism
prolonged immobility
excessive doses of vitamin D
medications
hypercalcemia manifestations
neuro = lethargic, behavioral changes, coma
CV = HTN, inc contractility, arrhythmias
GI = nausea, vomiting, constipation
GU = high output, renal calculi
phosphorus is needed for
bone formation
many cellular functions (ATP, metabolism, nucleic acids, phospholipid membrane formation)
acid-base buffer
normal WBC & platelets
hypophosphatemia
high phosphorus levels
hypophosphatemia symptoms
neuro, paresthesia, ataxia, confusion, stupor, coma, seiziures, tremors
musculoskeletal = joint stiffness, bone pain, osteomalacia
blood = hemolytic anemia, platelet dysfunction w/ bleeding, imapired WBC function
causes of hypophosphatemia
inadequate absorption in intestines
malnutrition (increases phosphate excretion)
alcohol abuse
diabetic ketoacidosis
hyperphosphatemia
high phosphorus levels
hyperphosphatemia symptoms
neuro = paresthesia, tetany
cv = hypotension, arrhythmias
causes of hyperphosphatemia
kidney failure
phabdomyolysis & massive tissue injury
hyperphosphatemia will cause
hypocalcemia
magnesium functions
required for cellular energy metabolism
functioning of Na/K pump
membrane stabilization
nerve conduction
ion transportation (K and Ca)
smooth muscle relaxant
hypomagnesemia symptoms
inc neuromuscular excitability = personality changes, weakness & tremors, hyperactive reflexes, seizures
CV = tachycardia, HTN, ventricular arrhythmias
causes of hypomagnesemia
diarrhea
prolonged NG suction
malnutrition & malabsorption
chronic alcoholism
hypermagnesemia symptoms
neuromuscular = lethargy, hyporeflexia & weakness, confusion, coma
CV = hypotension, arrhythmias, cardiac arrest