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81 Cards in this Set

  • Front
  • Back
Body fluids present in . . .?
in cells.
in the space b/t cells and outside blood vessels (interstitial).
in the blood vessels
Function of fluid?
maintain cell shape-
transport gases, nutrients, wastes-
generate electrical activity-
transform food into energy-
Fluid compartments?
Intracellular inside cell
Extracellular outside cell
a. interstitial
b. intravascular- fluid of blood.
c. transcellular- in CSF; and in spaces like the peritoneal, pleural, & pericardial cavities.
Total Body Water

muscle more than fat*
adult male 60% TBW
Adult female has less d/t (more fat)
Obese adults 45% TBW
Elderly adults 45% TBW d/t loss of muscle mass
TBW maintained by _____ & ______?
thirst and ADH hormone
ADH is?

acts on DCT for increased fluid re-absorption.
antidiuretic hormone, secreted by posterior pituitary, synthesized by hypothalamus. stimulates kidneys to reabsorb h2o when ECF volume is low
Electrolytes
substances that dissolve in solution to form ions (+ cation or - anion)
distribution depends on charge.
any + can transfer with another +
same goes for any -
ICF
contains 2/3 of TBW
potassium is major cation
largest compartment
ECF
contains 1/3 of TBW-
sodium is major cation but has other cations and anions.
Cl- is main ECF anion
its the ECF levels that are drawn for labs-
The distribution of electrolytes b/t body compartments is influenced by _______________?
their electrical charge-
Movement of H2O
osmosis, hydrostatic pressure, colloid osmotic pressure
Osmosis
fluid moves across a semi-permeable membrane (permeable to H2O) but little else).
moves along a gradient of higher to lower concentrations-
Hydrostatic Pressure
is the force of the fluid. the pushing force behind the fluid that can push H2O out
Osmolarity
concentration of molecules in the H2O
it can pull water
usual serum osmality is around 280-295 mOsm/kg, it can increase in volume deficits and decrease in volume excesses
Colloid Osmotic Pressure
osmotic pressure is the pulling force created by the stuff that cant pass through the membrane.
Isotonic IVF
concentration of particles is equal to ICF or ECF. 0.9% NaCl is the baseline for %; or 5% dextrose for example. will neither shrink nor swell the cells. Lactated Ringers (LR)
Hypertonic IVF
concentration of particles is greater than ICF so cells shrink b/c now there is more stuff in the ECF than the ICF. % of solutes will be higher than in baseline 0.9%-
3%NS, D5W in 1/2NS, D10W
Hypotonic IVF
concentration of dissolved particles is less than ICF so the cells swell b/c now there is more stuff in the ICF than there are in the ECF. % of solutes will be less than in 0.9%. ex. 0.45% or 1/2NS
Edema
accumulation of fluid within interstitial spaces. edema cant be visually observed until IFV has ^ 2.5 to 3X
Edema

Causes?
^ capillary hydrostatic pressure in excess fluid volume, some type of venous obstruction.
decreased capillary osmotic pressure in starvation, liver fail
^ capillary permeability: trauma, burns, inflammation
Edema

Types?
localized with inflammation, injury
thrombophlebitis-
generalized as a result of CHF
pulmonary-
dependent- usually in LE
lymphedema- blocked, or removed (mastectomy)
Edema

Assessments for . . .
daily wt. gain of 2.2 in 24h is concern
visual, compare sides, monitor I&Os, measure & compare, pitting or not, lung sounds
Sodium Balance
Na+, most abundant cation in body and in ECF, 135-145 mEq/L, helps regulate H2O, regulates osmolality, helps reg. acid/base b/c part of Na bicarb, nerve impulse,
Sodium Balance

regulated by?
reg. by the renin-angiotensin-aldosterone system.

aldosterone acts on 'late distal tubule'
to reabsorb Na+, H2O, and excrete K+
Hyponatremia
low serum sodium levels

less than 135 mEq/L
Hyponatremia

Causes?
H2O retention (hemodilution) common
loss of Na+ through skin, GI tract, kidneys
^ Na+ shift into cells-
diuretics,
Hyponatremia

How it presents?
ability to depolarize and repolarize affected: confusion, depressed reflex, seizures, coma, and SxS of fluid of volume overload
Hyponatremia

Treatment?
strict I&Os, loop diuretic use in volume excess, saline admin, if severe Na+ loss may require hypertonic solution administration.
Hypernatremia
increased ECF Na+ levels

higher than 145 mEq/L
Hypernatremia

Causes?
net gain of Na+, net loss of water
rapid infusion of Na+, thirst defect, loss of fluids that have low level Na+, hypodipsia (impaired thirst),
Hypernatremia

How it presents?
dry skin, dry M&Ms, lowered salivatory and tear production, or signs associated with fluid volume deficits, neuro signs for sure
Hypernatremia

Treatment?
focus on underlying cause
sodium restrict intake, oral hydration preferred
Potassium
normal level 3.5-5.5 mEq/L
major cation of ICF
most in muscle so losses occur with age as muscle mass loss
Potassium Balance

Regulation?
aldosterone - saves Na+ kicks K+
Insulin causes K+ to move from ECF back to cells-
Na+/K+ pump,
K+/H+ exchange system- K+ gets excreted in urine and gets replaced by H+ (one for one)
Hypokalemia
decreased serum K+ < than 3.5 mEq/L
Hypokalemia

Causes?
inadequate nutrition, excess loss @ GI tract or skin, diuretics (Loop), metabolic alkalosis promotes movement of K+ into cells in exchange for H+,
Hypokalemia

How it presents?
postural hypotension, EKG changes, arrhythmia, muscle weak & cramps, decrease GI motility, K+ is abundant in myocardium.
Hypokalemia

Treatment?
focus on underlying cause-
^ dietary intake- fresh fruit veggies, salt subs
K+ supplements-
IV K+CL- (NO IV PUSH FOR K+)
Hyperkalemia
serum K+ greater than 5.5 mEq/L
Hyperkalemia

Causes?
RF most common as decreased renal elimination.
cell injury leading to K+ into ECF
metabolic acidosis b/c of the relationship b/t K+ and H+!!!
rapid IV K+
Hyperkalemia

How it presents?
earliest symptom is paresthesias
general muscle weakness/dyspnea
EKG changes
Hyperkalemia

Treatment?
goals are to prevent complications, treat underlying cause(s)-
restrict K+ intake
Loop diuretics
kayexalate- med that assist with cation exchange
Hemodialysis
Insulin & glucose ^ cell uptake of K+
Calcium Ca+
serum range of 8.5-10.5 mg/dL
forms bone and teeth, assist in membrane permeability, impulse transmission, affects muscular contractions cardiac, smooth, and skeletal (it calms). promotes blood clotting b/c its required for all but 2 steps of the process
Calcium

Regulation?
reg by parathyroid gland, Calcitonin takes out of ECF, albumin levels b/c about 1/2 Ca+ is bound to the protein, Vitamin D needed to absorb Ca+
Phosphorus-inverse relationship
Hypocalcemia
Ca+ < than 8.5 mg/dL
Hypocalcemia

Causes?
intake issues, RF d/t to inability for kidney to activate vitamin D for Ca+ absorption and also leads to ^ phosph.
hypoparathyroidisim
diarrhea, lack of vitamin D, diuretics
Hypocalcemia

How it presents?
paresthesias, tetany, dysrythmias, fractures, bone pain, osteoporosis
^ risk of bleeding-
Hypocalcemia & Tetany

Tetany is involuntary muscle contractions-
Chvostek's sign is tapping on face under temple where facial nerve emerges to elicit twitch in lip, nose, etc.

Trousseau's sign uses BP cuff inflated for 3 minutes to look for contraction of fingers and hand.
Hypocalcemia

Treatment?
identify cause. if Tetany present IV Ca+ slowly. ^ oral intake of Ca+ & vitamin D.
Hypercalcemia

Causes?
serum Ca+ above 10.5 mg/dL

hyperparathyroidism, some CA produce ectopic PTH, prolonged immobilization
Hypercalcemia

How it presents?
decreased neuromuscular excitability, dull consciousness-even stupor
bradycardia & dysrythmias
constipation, possible Kx stones
Hypercalcemia

Treatment?
hydratation, loop diuretics
The Acid / Base balance system-
imbalances are due to changes in H+ concentration-

Acid is a molecule that release H+
Base is a molecule capable of combing with, or accepting H+
Carbonic Acid (H2CO2)

Bicarbonate (HCO3)
a weak acid derived from CO2

is a weak base-
pH and H+ have what kind of relationship?

Normal pH is 7.35 - 7.45
an inverse relationship-
a decrease in H+ raises pH = alkalosis

a ^ in H+ lowers pH = acidosis
Normal ABG values
pH is 7.35 - 7.45
< pH = acidosis, > pH = alkalosis
PaCO2 is 35 - 45
< PaCO2 = alkalosis
> PaCO2 = acidosis
HCO3 is 22-26
< HCO3 = acidosis
> HCO3 = alkalosis
AbNormal ABG values

When HCO3 is mostly affected it is of a metabolic origin-
Metabolic Alkalosis is characterized by pH > 7.45 & HCO3 > 26
AbNormal ABG values

When PaCO2 is mostly affected it is of a respiratory origin-
Respiratory Acidosis is characterized by pH < than 7.35 & PaCO2 > 45
Respiratory Alkalosis is characterized by pH > 7.45 & PaCO2 < 35
Acid / Base

Regulators, how many mechanisims? What are they?
3 systems.
ICF & ECF chemical buffers
Respiratory system
Kidneys/Renal system
ICF & ECF chemical buffers
immediate effects-

Protein buffer system
Protein Buffer System
largest system in body, immediate effect, Fx as either acid or base, located within cells mostly H+ & CO2 diffuse across membrane by intracellular proteins.
ICF & ECF chemical buffers

Bicarbonate buffer system
uses H2CO3 (carbonic acid) as its weak acid and HCO3 (bicarb) as its weak base. very efficient system.
ICF & ECF chemical buffers

H+ & K+ exchange system
can move freely b/t cells and exchange from ICF to ECF.
Respiratory system
PaCO2 of 35 - 45 normal
effects within minutes to hours
When metabolic imbalance the compensatory mech. is respiratory-
works through elimination or holding of CO2.
hypoventilation 'holding of CO2' decreases pH = acidosis.
hyperventilation 'blowing off CO2'
increases pH = alkalosis
Renal System
HCO3 of 22-26 mEq/L normal
makes long term adjustments in pH-
not immediate, but long lasting effect-
makes its long term adjustments to pH by producing and reclaiming bicarb and through the reabsorbing and/or excreting of H+
Renal System

When there is a respiratory imbalance the compensatory mechanism is the metabolic pathway-
the kidneys will produce or reclaim bicarb and excrete or reabsorb H+
Metabolic Acidosis

Characterized by?
pH < than 7.35 &
HCO3 < than 22 mEq/L
Metabolic Acidosis

Causes?
^ production/ingestion of acids
excess lactic acid production that occurs w/ exercise, shock, cardiac arrest; Renal failure, ^ bicarb loss through diarrhea, gut suctioning; ketoacidosis
Metabolic Acidosis

How it presents?
marked to progressive weakness, fatigue, progressing to coma or stupor-
dysrythmias, N&V, abdm pain, increased respirations rapid and deep
'Kussmaul's respirations
Metabolic Acidosis

Treatment?
compensatory is ^ respirations rapid and deep (although not exactly an immediate occurrence) to blow off more CO2 and increase pH -
may give sodium bicarb-
monitor K+ b/c of the rapid effects of the exchange buffer system with H+
mechanical ventilation as needed-
Metabolic Alkalosis

Characterized by?
pH > than 7.45 &
HCO3 > than 26 mEq/L
Metabolic Alkalosis

Causes?
excess bicarb intake-
^ bicarb retention-
excess H+ dumping d/t vomiting or NG suction-
Metabolic Alkalosis

How it presents?
many are asymptomatic-
respirations slow and shallow to hold more CO2 to decrease the pH-
SxS of hypokalemia: ekg changes, postural hypotension, muscle cramp, decrease GI motility
Metabolic Alkalosis

Treatment?
monitor for decreased serum K+ b/c of exchange buffer system with H+
correct cause-
KCl & IV fluids,
Respiratory Acidosis

Characterized by?
pH < than 7.35 &
PaCO2 > 45 mm Hg
Respiratory Acidosis

Causes?
Acute: narcotic OD (depressed RR), lung diseases, chest injuries, airway obstructions, anything that can impair good gas exchange:
Chronic: COPD, Carbohydrate rich diets (they produce large amounts of CO2)
Respiratory Acidosis

How it presents?
SxS related to hypoxemia leading to hypoxia- restlessness & anxiety, progressing to decreased level of consciousness to coma- increase ICP d/t cerebral vasodilation r/t hypercapnia
tachycardia, diaphoresis, rapid shallow respirations. Cyanosis as a late sign-
Respiratory Acidosis

Treatment?
improve ventilation, correct underlying cause if can:
Compensation for an acute respiratory acidosis is by intracellular buffering with proteins and phosphates. Compensation for chronic, or more long term is renal retention of bicarbs.
Respiratory Alkalosis

Characterized by?
pH > than 7.45 &
PaCO2 < 35 mm Hg
Respiratory Alkalosis

Causes?
hyperventilation as with panic attacks, anxiety, severe pain, and fever, etc.
blowing off too much CO2:
hypoxemia, pneumonia, and other things that cause increased respirations
Respiratory Alkalosis

How it presents?
restlessness, anxiousness, dizziness,
decreased ICP, eventual inhibition of respiratory drive d/t lowered CO2 (CO2 is the stimulant to breathe), cerebral vasoconstriction, cardiac arrhythmias, decrease myocardial contractility, hypocalcemia
Respiratory Alkalosis

Treatment?
O2 to prevent hypoxemia, correct underlying cause, breath in bag,