fluids and electrolytes Flashcards
intracellular volume is what percent of total body weight?
40% (28L)
extracellular volume is what percent of total body weight? (including its makeup and %)
20% (14L)
16% is ISF
4% is plasma volume
what is the net filtration pressure equation?
(capillary hydrostatic pressure- interstitial hydrostatic pressure) - (interstitial oncotic pressure - capillary oncotic pressure)
osmotic pressure
pressure of a solution across a semi permeable membrane that prevents water from diffusing across that membrane
how do you calculate plasma osmolarity and what is normal
normal is 280-290
=2(Na)+(glucose/18)+(BUN/2.8)
what can increase plasma osmolarity
hyperglycemia and uremia
name two hypotonic solutions
D5W, NaCl .45%
name 6 isotonic solutions
NS, LR, plasmalyte A, albumin 5%, voluten 6%, vespan 6%
name 5 hypertonic solutions
NaCl 3%
D5 NaCl .9%
D5 NaCl .45%
D5 LR
Dextran 10%
how does hypotonic solution affect osmolarity, ECF, and ICF
increases ECF and ICF volumes and decreases osmolarity
how does isotonic solution affect osmolarity, ECF, and ICF
increases ECF, but ICF and osmolarity stay the same
how does hypertonic solution affect osmolarity, ECF, and ICF
giving hypertonic fluid expands intravascular volume by pulling fluid from ICF to ECF- ECF and plasma osmolarity increase but ICF decreases
what does albumin bind to
calcium and it causes hypocalcemia
which is the most abundant intracellular cation
potassium
hypokalemia presentation
skeletal muscle cramps –> weakness –> paralysis –> worsens digitalis toxicity
hyperkalemia presentation
cardiac rhythm disturbances
hypokalemia EKG findings
PR interval and QT interval are longer
flat T wave
U wave
hyperkalemia EKG findings
(based on serum K concentration)
5.5-6.5 peaked T waves
6.5-7.5 p wave flattening, PR prolongation
7-8 QRS prolongation
8.5 or greater QRS–>sine wave –> VF
what is the most abundant extracellular cation
sodium
etiologies of hyponatremia (3 categories)
decreased total body Na content (diuretics, salt wasting disease, hypoaldosteronism)
normal total body sodium content (SIADH, hypothyroidism, water intoxication, preoperative stress)
increased total body Na content (cirrhosis, CHF)
etiologies of hypernatremia (3 categories)
decreased total body Na content (osmotic diuresis, n/v, adrenal insufficiency)
normal total body Na content (DI, renal failure, diuretics)
increased total body Na content (hyperaldosteronism, increased sodium intake like 3% saline)
presentation of hyponatremia
130-135
125-129
115-124
<115
based on serum Na concentration
130-135 no signs to mild signs
125-129 n/v, malaise
115-124 HA, lethargy, altered LOC
115 or less (rapid onset) seizures, coma, cerebral edema, respiratory arrest
presentation of hypernatremia
based on serum osmolality
350-375 HA, agitation, confusion
376-400 weakness, tremors, ataxia
401-430 hyperreflexia, muscle twitching
431 or more: seizures, coma, death
normal plasma calcium (total) in mg/dL, mEq/L, mmol/dL
8.5-10.5 mg/dL
4.5-5.5 mEq/L
2.12-2.62 mmol/dL
normal plasma calcium (ionized) in mg/dL, mEq/L, mmol/dL
4.65-5.28 mg/dL
2.2-2.6 mEq/L
1.16-1/32 mmol/dL
how much calcium is ionized
50%
which is the most abundant electrolyte in the body
calcium
which hormone raises serum calcium and which hormone decreases serum calcium
PTH increases, calcitonin decreases
etiologies of hypocalcemia (5)
hypoparathyroidism
vitamin D deficiency
renal osteodystrophy
pancreatitis (same reason as sepsis, increased circulating catecholamines shifts ca into intracellular compartment)
sepsis
etiologies of hypercalcemia
hyperparathyroidism
cancer
thyrotoxicosis
thiazide diuretics (increases ca reabsorption în exchange for Na)
immobilization
presentation of hypocalcemia
skeletal muscle cramps
nerve irritability- parasthesia and tetany
laryngospasm
mental status changes- seizures
chovsteks sign (facial nerve/masseter muscle)
trusseaus sign (BP inflated above SBP for 3 min, muscle spasms of hand and arm)
presentation of hypercalcemia
nausea
abdominal pain
HTN
psychosis
mental status changes - seizures
EKG finding with hypocalcemia
long QT interval (prolonged plateau phase of AP)
EKG finding with hypercalcemia
short QT interval
treatment of hypocalcemia
calcium or vitamin D
treatment of hypercalemia
NS or loop diuretic (furosemide)
normal plasma magnesium (mg/dL and mEq/L)
1.7-2.4mg/dL or 1.5-3mEq/L
etiology of hypomagnesemia (5)
poor intake
alcohol abuse
diuretics
critical illness
common with hypokalemia (will cause K efflux at renal level) and usually also tells PTH to chill which decreases Ca as well
etiology of hypermagenesemia (3)
excessive administration
renal failure
adrenal insufficiency (addisons aka low cortisol and aldosterone output, which increases tubular magnesium reabsorption)
treatment for hypermagnesemia
calcium chloride or gluconate
symptoms of a magnesium level <1.2mg/dL
tetany, seizures, dysrhythmias
symptoms of a magnesium level between 1.2-1.8mg/dL
neuromuscular irritability
hypokalemia
hypocalcemia
symptoms of a magnesium level between 2.5-5mg/dL
typically none
symptoms of a magnesium level between 5-7mg/dL
diminished DTR’s
lethargy/drowsiness
flushing
n/v
symptoms of a magnesium level between 7-12mg/dL
loss of DTR’s
hypotension
EKG changes
somnolence
symptoms of a magnesium level >12mg/dL
respiratory depression- apnea
complete heart block
cardiac arrest
coma
paralysis
cardiac, CNS, pulmonary, other effects of acidosis include
increased p50 (right = release)
increased SNS tone
increased risk of dysrhythmias
decreased contractility
increased cerebral BF
increased ICP
increased PVR
hyperkalemia
cardiac, CNS, pulmonary, other effects of alkalosis include
decreased p50 (left=love)
decreased coronary blood flow
increased risk of dysrhythmias
decreased CBF
decreased ICP
decreased PVR
hypokalemia
decreased ical (promotes binding of calcium to albumin)
for acute respiratory acidosis, for every 10mmHg increase in PaCO2, pH decreases by
.08
for chronic respiratory acidosis, for every 10mmHg increase in PaCO2, pH decreases by
.03
anion gap equation
major cations - major anions OR
Na - Cl + HCO3= 8-12mEq/L
etiology of anion gap acidosis (>14 gap)
MUDPILES
methanol
uremia
DKA
paraldehyde
isionazid
lactate
ethanol, ethylene glycol
salicylates (inhibits krebs cycle)
etiology of non gap acidosis
HARDUP
hypoaldosteronism
acetazolamide
renal tubular acidosis
diarrhea
ureterosigmoid fistula
pancreatic fistula
for every HCO3 decrease of 1mEq/L, PaCO2 decreases by
1-1.5mEq/L
metabolic alkalosis etiologies
sodium bicarb administration
massive transfusion (liver converts preservatives to HCO3-)
loss of gastric fluid (most common)
loss of acid in urine
diuretics
ECF depletion (–>increased Na reabsorption –> H and K excretion (maintains electroneutrality))
cushings syndrome (activation of mineralocorticoid receptors by increased cortisol causes Na reabsorption and K secretion and metabolic alkalosis)
hyperaldosteronism (conns disease, increases Na retention and hydrogen ion excretion)
treatment of metabolic alkalosis
acetazolamide (carbonic anhydrase inhibitor, increases renal excretion of HCO3)
spironolactone (mineralocorticoid antagonist)
dialysis
fluid replacement per hour for very minimal surgical trauma (orofacial surgery)
1-2mL/kg/h
fluid replacement per hour for minimal surgical trauma (inguinal hernia repair)
2-4mL/kg/h
fluid replacement per hour for moderate surgical trauma (major nonabdominal surgery)
4-6mL/kg/h
fluid replacement per hour for severe surgical trauma (major abdominal surgery)
6-8mL/kg/h
4:2:1 rule
4mL/kg/h for first 10kg body weight
2mL/kg/h for second 10kg of body weight
1mL/kg/h for anything over that
