Unit 9 - Fluids & Electrolytes Flashcards
what is the plasma volume of a 70 kg male
3 L
total body water of 70 kg male
42 L
body water distribution in 70 kg male
60/40/20 (15/5)
water = 60 % TBW
ICF = 40% TBW (28 L)
ECF = 20% TBW (14 L)
interstitial fluid = 15% (11L)
plasma fluid = 5% (3L)
components of extracellular fluid
interstitial fluid (11L)
plasma (3 L)
major ions of ICF
K+, Mg2+, PO42-
major ions of ECF
Na+, Ca2+, Cl-, HCO3-
volume of ICF vs ECF
ICF = 40% of TBW or 28 L
ECF = 20% of TBW or 14 L
population differences in TBW
- Neonates have higher TBW % by weight
- Females, the obese, and the elderly have a lower TBW % by weight
what is plasma volume
non-cellular fraction of circulating blood volume
what determines net movement of fluid between intravascular & interstitial spaces
Starling forces & glycocalyx
what are starling forces
dictate passive exchange of water between capillaries and interstitial fluid
forces that move from capillary to interstitial space and vice versa
starling forces: Pc
Pc = capillary hydrostatic pressure (pushes fluid out of capillary)
Starling forces: π if
π if = interstitial oncotic pressure (pulls fluid out of capillary)
Starling forces: Pif
Pif = interstitial hydrostatic pressure (pushes fluid into capillary)
Starling forces: π c
π c = capillary oncotic pressure (pulls fluid into capillary)
how do fluids tend to be pulled back into the capillary
capillary oncotic pressure
how is fluid pushed out as it enters the capillary
capillary hydrostatic pressure
net filtration pressure =
(Pc - Pif) - (πc - πif)
NFP > 0 =
NFP < 0 =
> 0 = filtration (fluid exits capillary)
< 0 = reabsorption (fluid pulled into capillary)
Gatekeeper that determines what can pass from vessel into interstitial space
Glycocalyx
Conditions that impair glycalyx integrity
sepsis
ischemia
DM
major vascular surgery
function of glycocalyx
- forms a protective layer on the interior wall of blood vessel
- determines what can pass from vessel to interstitial space
blood volume =
sum of plasma volume and blood cell volume (60% plasma & 40% blood)
what is Hct
the fraction of blood volume occupied by erythrocytes
how is Hct increased
by increased # RBCs (polycythemia) or decreased plasma volume (hypovolemia)
how is Hct decreased
by decreased # RBCs (anemia) or increased plasma volume (hemodilution)
why are erythrocytes considered part of intracellular compartment
filled with fluid but considered part of intracellular compartment bc contained by a membrane
what is the interstitium
space between cells
what makes up nearly all of interstitial “fluid”
gel consisting of fluid & proteoglycan filaments
fluid movement in the interstitium is a function of:
diffusion
fluid scavenger that removes fluid, protein, bacteria, & debris that has entered the interstitium
Lymphatic System
how does the lymphatic system propel lymph
pumping mechanism
how does the lymphatic system affect pressure in interstitial space
Produces net negative pressure in interstitial space
what causes edema in regards to the lymphatic system
occurs when rate of interstitial fluid accumulation exceeds rate of removal by lymphatic system
how is lymph returned to venous circulation
via thoracic duct at juncture of IJ & subclavian
why is left IJ CVL insertion assoc. with greater risk of chylothorax
thoracic duct is larger on the left
how do most solutes get across semipermeable membranes separating the body’s compartments
carrier proteins transport these solutes from one side to another
what is osmosis
net movement of water across a semipermeable membrane (only water, not solute, can pass through membrane)
what drives direction of water movement via osmosis
difference in solute concentration on either side of membrane
Water tends to move from areas of lower solute to areas of higher solute concentration
what is diffusion
net movement of a substance from area of higher concentration to area of lower concentration across fully permeable membrane
pressure of a solution against a semipermeable membrane, prevents water from diffusing across that membrane
Osmotic pressure
what is osmotic pressure a function of
the number of osmotically active particles in a solution
NOT a function of molecular weights
number of osmoles per liter of solution
osmolarity
mOsm/L of total solution
number of osmoles per liter of solution
osmolarity
mOsm/L of total solution
number of osmoles per kg of solution
osmolarity
mOsm/kg of H2O
number of osmoles per kg of solution
osmolarity
mOsm/kg of H2O
number of osmotically active particles in a solution
osmole
normal plasma osmolarity
280-290 mOsm/L
Most important determinant of plasma osmolarity
Na+
how do hyperglycemia or uremia affect plasma osmolarity
can increase
helps us understand how different IV solutions impact volumes of ECF & ICF as well as plasma & cellular osmolarity
Dannow-Yannet Diagrams
what happens to cells in hypotonic solutions
water enters, cells swell
what happens to cells in hypertonic solutions
water exits, cells shrink
it is assumed that addition or loss of fluid occurs where?
in ECF
osmolarity of hypotonic solutions vs plasma
lower than plasma
how do hypotonic solutions affect ECF, ICF, and plasma osmolarity
↑ ECF & ICF volumes
↓ plasma osmolarity
why should a patient with increased ICP never receive a hypotonic solution
These fluids are akin to giving free water, which distributes throughout all body compartments
examples of hypotonic solutions
D5W
NaCl 0.45%
osmolarity of isotonic solutions vs plasma
Osmolarity approximates plasma (or cells)
how do isotonic solutions affect ECF, ICF, plasma volume, and plasma osmolarity
expand plasma volume & ECF (ICF and plasma osmolarity stay the same)
how do isotonic solutions affect ECF, ICF, plasma volume, and plasma osmolarity
expand plasma volume & ECF (ICF and plasma osmolarity stay the same)
how long do crystalloids tend to remain in intravascular space
~30 min
adverse effect of large amounts of NS
hyperchloremic metabolic acidosis
how does LR reduce risk of metabolic acidosis
Lactate in LR functions as a buffer
Lactate is converted to bicarb by liver & kidneys
Bicarb reduces risk of metabolic acidosis
what fluids can be used to dilute PRBcs
NS or Plasmaylte
(LR historically avoided but research shows that LR can be used safely when rapidly infusing PRBCs)
examples of isotonic solutions
- NaCl 0.9%
- Hespan 6%
- Plasmalyte A
- Albumin 5%
osmolarity of hypertonic solutions vs plasma
Osmolarity exceeds plasma (or cells)
how do hypertonic solutions affect intravascular volume, ECF, ICF, and plasma osmolarity
- expand intravascular volume by pulling fluid from ICF into ECF
- ECF & plasma osmolarity ↑
- ↓ ICF
consequence of increasing serum Na+ too quickly
central pontine myelinolysis
examples of hypertonic solutions
- 3% NS
- D5LR
- D5NS 0.9%
- D5NS 0.45%
- Dextran 10%
blood replacement volume with crystalloids
3:1
how long can crystalloids expand plasma volume
for 20-30 min
effects of dilution with crystalloids
dilutional coagulopathy
dilution of albumin = decreased capillary oncotic pressure
how long can colloids increase plasma volume
3-6 hours
effects of dextran 40
↓ blood viscosity
improves microcirculatory flow in vascular surgery
FDA black box warning on synthetic colloids
risk renal injury
coagulopathy with synthetic colloids
dextran > Hetastarch > Hextend
max volume of synthetic colloids
max 20 mL/kg
which colloid has the highest anaphylactic potential
dextran
synthetic colloid that does not have a problem with coagulopathy
Volvuven
only colloid that is derived from human blood products
albumin
Vd of albumin
approximates plasma volume
electrolyte imbalance possible with albumin
hypocalcemia (binds calcium)
normal serum potassium
3.5 - 5.5 mEq/L
plasma osmolarity calculation
conditions that increase osmolarity
hypernatremia
hyperglycemia
uremia
colloid that impairs ability to cross-match blood
dextran
which expands ECF - crystalloids or colloids?
crystalloids only
Most common electrolyte disorder in clinical practice
hypokalemia
Most abundant intracellular cation
K+
electrolyte that regulates RMP in nervous tissue, skeletal muscle, and cardiac muscle
K+
responsible for maintaining intracellular distribution of K+
Na-K-ATPase
Most important ion during repolarization of neural tissue & muscle cells
K+
GI losses that can result in hypokalemia
- V/D
- NG suction
- Zollinger-Ellison syndrome
- jejunoileal bypass
- kayexalate
4 etiologies of hypokalemia
- diet (poor K+ intake)
- GI loss
- renal loss
- redistribution
causes of renal loss of K+
- diuretics
- metabolic alkalosis
- licorice (can cause pseudo-Conn’s syndrome)
causes of hypokalemia from redistribution
(K+ shift intracellular)
- insulin + D50
- hyperventilation
- bicarb
- beta 2 agonists
- hypokalemic periodic paralysis
presentation of hypokalemia
skeletal muscle cramps
weakness
paralysis
EKG findings with hypokalemia
- long PR
- long QT
- flat T wave
- U wave
why is assessing total body K+ with a serum K+ often inaccurate
~98% of total body K+ is stored inside cells
why is it important to evaluate cause of hypokalemia before treating
If due to intracellular redistribution, supplemental K+ could lead to lethal hyperkalemia when cause of redistribution resolves
max rate of potassium infusion
PIV = 10 mEq/hr
CVL = 20 mEq/L
5 etiologies of hyperkalemia
- increased intake
- impaired excretion
- redistribution
- cellular injury
- pseudohyperkalemia
causes of impaired K+ excretion that can lead to hyperkalemia
- acute oliguric renal failure
- hypoaldosteronism
- drugs that impair K+ excretion (NSAIDs, spironolactone, triamterene)
drugs that impair K+ excretion
NSAIDs, spironolactone, triamterene
causes of K+ redistribution that contribute to hyperkalemia
K+ shifts extracellularly
- acidosis
- succinylcholine
- beta blockers
- hyperkalemic periodic paralysis
causes of cellular injury that contribute to hyperkalemia
- tumor lysis
- hemolysis
- burns
- crush injury
- rhabdo
EKG findings with hyperkalemia
- 5.5-6.5 = peaked T waves
- 6.5-7.5 = flat P wave, prolonged PR
- 7.0-8.0 = prolonged QRS
- > 8.5 = QRS - sine wave - V-fib
serum K level associated with sine wave
8.5 or greater
serum K+ assoc. with peaked T waves
5.5-6.5 mEq/L
treatment of hyperkalemia
- stabilize cardiac membrane with calcium
- shift K intracellularly (insulin + D50, hyperventilation, bicarb, beta 2 agonist)
- K+ elimination with K+ wasting diuretics, kayexelate, dialysis
normal serum Na+
135-145 mEq/L
Most abundant extracellular cation
Na+
Primary determinant of serum osmolarity
Na+
Plays important role in regulating ECF volume through osmotic forces
Na+
when is Na+ most important
during depolarization of neural tissues and muscle cells
how is Na+ homeostasis regulated
- GFR
- renin-angiotensin-aldosterone system
- ANP/BNP
consider delaying surgery if Na+ is <
130
the serum Na+ concentration should be corrected no faster than:
2 mEq/L/hr
consequence of treating hyponatremia too quickly
- causes fluid to shift from ICF to ECF
- can cause central pontine myelinolysis
consequence of treating hypernatremia too quickly
causes fluid to shift from ECF to ICV
can cause cerebral edema
serum Na+ that defines hyponatremia
< 135 mEq/L
causes of hyponatremia related to decreased total body Na+ content
- diuretics
- salt-wasting disease
- hypoaldosteronism
causes of hyponatremia with normal total body Na+ content
- SIADH
- hypothyroid
- water intoxication
- periop stress
causes of hyponatremia assoc with increased total body Na+ content
CHF
cirrhosis
presentation of hyponatremia
- 130-135 = no signs to mild signs
- 125-129 = N/V, malaise
- 115-124 = headache, lethargy, altered LOC
- < 115 (rapid onset) = seizures, coma, cerebral edema, respiratory arrest
s/s hyponatremia at 125-129 mEq/L
N/V
malaise
s/s hyponatremia at 125-129 mEq/L
HA
lethargy
altered LOC
Na+ level assoc with seizures and cerebral edema
< 115 mEq/L
hyponatremia treatment
goal is to restore Na+ balance by manipulating serum osmolality and fluid balance with H2O restriction, IVF selection based on tonicity, and diuretics
serum Na+ in hypernatremia
> 145
etiologies of hypernatremia assoc with decreased total body Na+ content
- osmotic diuresis
- N/V
- adrenal insufficiency
causes of hypernatremia assoc with normal total body Na+ content
diabetes insipidus
renal failure
diuretics
causes of hypernatremia assoc with increased total body Na+ content
hyperaldosteronism
↑ intake (3% saline)
what determines presentation of hypernatremia
serum osmolality
serum Na+ concentration determines presentation with hyponatremia
what determines presentation of hypernatremia
serum osmolality
serum Na+ concentration determines presentation with hyponatremia
presentation of hypernatremia
depends on serum osmolality
* 350-375 = headache, agitation, confusion
* 376-400 = weakness, tremors, ataxia
* 401-430 = hyperreflexia, muscle twitching
* > 431 = seizures, coma, death
normal total plasma calcium
8.5 - 10.5 mg/dL
4.5 - 5.5 mEq/L
or 2.12 - 2.62 mmol/dL
normal ionized plasma calcium
4.65-5.28 mg/dL
2.2-2.6 mEq/L
or 1.16-1.32 mmol/dL
Calcium:
____ % is ionized
____% is bound to albumin
____% is bound with an anion
50% is ionized
40% is bound to albumin
10% is bound with an anion
Most abundant electrolyte in the body
calcium
where is nearly all calcium stored
in bone
serves as a reservoir for maintaining plasma calcium level
where is nearly all calcium stored
in bone
serves as a reservoir for maintaining plasma calcium level
important functions of calcium
- 2nd messenger systems
- neurotransmitter release
- muscular contraction
- phase 2 of cardiac muscle cell AP
- factor 4 in coagulation pathway
Antagonizes effects of Mg2+ at NMJ
calcium
how does acidosis affect ionized calcium
increases
(albumin binds H+ and displaces Ca2+ into plasma)
how does alkalosis affect ionized calcium
decreases
(albumin binds Ca2+ and displaces H+ into the plasma)
how does parathyroid hormone affect serum calcium
increases
how does calcitonin affect serum calcium
decreases
osteoclast activity with increased serum calcium level
inhibited
what releases calcitonin in response to increased calcium level
thyroid
parathyroid response to decreased calcium level
releases PTH
how does the body respond to decreased calcium levels
- parathyroid glands release PTH
- osteoclasts release calcium from bone
- calcium reabsorbed by kidneys
- increased calcium absorption in small intestine (via vitamin D synthesis)
etiologies of hypocalcemia
- hypoparathyroidism
- vitamin D deficiency
- renal osteodystrophy
- pancreatitis
- sepsis
presentation of hypocalcemia
- skeletal muscle cramps
- nerve irritability (paresthesia & tetany)
- laryngospasm
- AMS
- seizures
- Chvostek sign
- Trousseau sign
what phase of cardiac AP is calcium responsible for
phase 2 (plateau)
which factor is calcium in the coagulation pathway
factor 4
EKG findings of hypocalcemia
long QT
serum calcium in hypocalcemia
< 8.5 mg/dL
serum calcium in hypercalcemia
> 10.5 mg/dL
etiologies of hypercalcemia
hyperparathyroidism, cancer, thyrotoxicosis, thiazide diuretics, immobilization
presentation of hypercalcemia
- nausea
- abd pain
- HTN
- psychosis
- AMS - seizures
Chvostek sign
tapping on jaw of facial n./masseter muscle causes ipsilateral facial contraction
trousseau sign
upper extremity BP cuff inflated above SBP for 3 minutes = decreased blood flow accentuates neuromuscular irritability = muscle spasms of hand and forearm
electrolyte imbalance assoc with short QT
hypercalcemia
hypercalcemia treatment
0.9% NaCl, Lasix
normal total plasma magnesium level
1.7-2.4 mg/dL or 1.5-3 mEq/L
where is Mg contained
Only 1% of total body Mg resides in ECF (0.3% in plasma)
The rest is contained intracellularly (mostly muscle and bone)
serum Mg may not correlate with total body Mg
where is Mg contained
Only 1% of total body Mg resides in ECF (0.3% in plasma)
The rest is contained intracellularly (mostly muscle and bone)
serum Mg may not correlate with total body Mg
antagonizes effects of calcium
Mg
Required for DNA synthesis, essential cofactor in many enzymatic functions
magnesium
where is most Mg reabsorbed
renal tubules
what hormone raises serum calcium
parathyroid hormone
what hormone decreases serum calcium
calcitonin
serum Mg level assoc with loss of DTRs
7-12 mg/dL or 5.8-10 mEq/L
dose of mag for preeclampsia
4g IV load over 10-15 minutes then 1 g/hr for 24 hours
clinical uses of mag
- Opioid-sparing techniques (NMDA receptor antagonism)
- Acute bronchospasm
- Cardiac rhythm disturbances: symptomatic PVCs or torsades de pointes
neonatal risks of magnesium infusion
Mg crosses placenta
admin > 48h increases risk of neonatal respiratory depression, hypotension, & lethargy
how does magnesium affect NMB
Hypermagnesemia can potentiate NMB with succs and nondepolarizers
what should you assess in an OB patient receiving mag for preeclampsia
loss of DTRs
etiologies of hypomagnesemia
- poor intake
- alcohol abuse
- diuretics
- critical illness
- common with hypokalemia
serum Mg that defines hypomagnesemia
< 1.8 mg/dL or < 1.5 mEq/L
presentation of Mg < 1.2 mg/dL (or < 1 mEq/L)
- tetany
- sz
- dysrhythmias
s/s Mg 1.2-1.8 mg/dL or 1-1.5 mEq/L
- neuromuscular irritability
- ↓ K+
- ↓ Ca2+
EKG findings with hypomagnesemia
not significant unless very low (long QT)
treatment of hypomagnesemia
mag sulfate supplementation
serum Mg in hypermagnesemia
> 2.5 mg/dL or > 2.1 mEq/L
etiologies of hypermagnesemia
- excessive admin
- renal failure
- adrenal insufficiency
s/s hypermagnesemia:
5-7 mg/dL
decreased DTRs
lethargy/drowsiness
flushing
N/V
s/s hypermagnesemia:
7-12 mg/dL
- loss of DTRs
- ↓ BP
- EKG changes
- somnolent
s/s hypermagnesemia:
> 12 mg/dL
- resp depression - apnea
- complete heart block
- cardiac arrest
- coma
- paralysis
magnesium levels assoc with dysrhythmias
< 1.2 mg/dL or > 7 mg/dL
treatment of hypermagnesemia
CaCl or CaGluconate
4-2-1 rule for calculating fluid maintenance
- 4 mL/kg/hr for first 10 kg body weight
- 2 mL/kg/hr for second 10 kg body weight
- 1 mL/kg/hr for each subsequent kg of body weight
For an adult, can use body weight in kg + 40 mL
4-2-1 rule for calculating fluid maintenance
- 4 mL/kg/hr for first 10 kg body weight
- 2 mL/kg/hr for second 10 kg body weight
- 1 mL/kg/hr for each subsequent kg of body weight
For an adult, can use body weight in kg + 40 mL
calculating fluid deficit
fasting hours x calculated hourly IVF rate
third space replacement
- Very minimal surgical trauma (ex. orofacial surgery): replace 1-2 mL/kg/hr
- Minimal surgical trauma (ex. inguinal hernia): replace 2-4 mL/kg/hr
- Moderate surgical trauma (ex. major nonabdominal surgery): replace 4-6 mL/kg/hr
- Severe surgical trauma (ex. major abdominal surgery): replace 6-8 mL/kg/hr
existence of third space is controversial
why is UOP an unreliable measure of fluid status
ADH reduces the kidney’s ability to eliminate fluid
fundamental objective of goal directed fluid therapy
optimizing O2 delivery
how does inadequate or excessive fluid affect O2 delivery
- Inadequate circulating volume reduces CO and O2 delivery
- Excessive circulating volume promotes microvascular congestion (also impairs O2 delivery)
which area of the starling curve best correlates with preload dependence
slope (ascending limb)
key principle of goal directed fluid therapy
admin. of small quantities of fluid (~200-250 mL) to determine the difference between preload dependence and preload interdependence
what does plateau of Starling curve suggest
- Suggests an optimal balance between circulating volume and myocardial performance
- Additional fluid would not be expected to improve hemodynamics or O2 delivery and might cause harm by pushing the patient further right on the curve
risks of overshooting the Starling curve
CHF
pulmonary edema
ERAS was originally designed for what types of surgeries
colon
3 most important determinants of plasma osmolarity
- Na+
- BUN
- glucose
consequence of correcting hyponatremia too quickly
osmotic demyelination syndrome
more common when hyponatremia persisted > 48 hrs
consequence of correcting hyponatremia too quickly
osmotic demyelination syndrome
more common when hyponatremia persisted > 48 hrs
sodium concentration of solutions containing 0.9% NaCl
includes 5% albumin, NS, D5NS
154 mEq/L
sodium concentration of 5% albumin
154 mEq/L
which IVF is most physiologic
plasmalyte (Na+ 140)
Na+ concentration of LR-containing solutions
130 mEq/L
includes LR and D5LR
