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82 Cards in this Set

  • Front
  • Back
*Isotonic solutions
-AKA as balanced
-AKA crystalliod
solute concentration is SAME between solutions so there is no shift

"stay where I put it"

USES: fluid lost outside of body

ALERT: raises B/P !!
-can cause HTN, FVE, hypernatremia
-not used w/HTN, cardiac/renal dz

EXAMPLES:
-NS
-LR
-D5W and D5 1/2 NS (until sugar used)
*Hypotonic solutions
HYPO=LESS solutes so fluid moves OUT of this solution into cells

hyOtonic =goes Out of the vessel
and DO NOT cause HTN

USES:
-those w/FVD w/HTN
and/or hx of renal/cardiac dz
-tx hypernatremia
-tx cellular dehydration

ALERT: cellular/cerebral edema
-can cause FVD and decreased BP
-be careful w/head injury and infants
EXAMPLES:
-tapwater
-anything less concentrated than isotonic
-also D5W after glucose is used
*Hypertonic solutions
-AKA Colloid

HYPER=MORE solutes so fluid moves INTO this solution (think packed particles)

hypertonic=Enter the vessel
-this shrinks cells

USES:
-tx hyponatremia
-tx 3rd space fluid shifts
-pt w/FVE but needs electrolytes
(ie, HF, edema, etc)

ALERT: FVE
-monitor in ICU, BP and CVP,etc

EXAMPLES:
-5% dextrose in normal saline
D10W, NS3-5%, D5W in 0.9%NS, D5W in 0.45% NS, D5W in LR, TPN, Albumin
Diffusion
solutes move from area of high concentration to area of low

-no energy needed=passive transport
-SOLUTES move

-uses Kinetic energy
(Brownian Motion)=the bump
Osmosis
fluid moves from an area of high fluid concentration to area of low fluid concentration

-no energy needed=passive transport
-FLUID moves (the ONLY way )
Active transport
energy via adenosine triphosphate (ATP)
moves solutes from an area of lower concentration to an area of higher concentration

-and ATP requires O2
Na-potassium pump
-There is more NA outside the cell
(ECF)
-and more K inside the cell (ICF)

-they want to move by diffusion but this pump keeps them in check
*what is the minimum amount of urine that should be seen
1cc per kg per hour
*ADH

what is it

where is it made and stored

what triggers release

what effects does it have

what blocks or stops release
-AKA vasopressin
-AKA Antidiuretic hormone

-peptide hormone
-made by hypothalamus
-stored in posterior pituitary
-released when serum osmolality is high (>300)
....and later by low BP
-osmoreceptors in hypothalamus sense the change in osmolality

1)causes distal tubule of nephron to keep WATER
2) also causes peripheral vascular constriction
=both increase fluid volume/BP

-alcohol, ANP, and angiotensin II block its release
thirst

2 types and which is activated 1st and by what
center located in hypothalamus

2 types:
-osmotic thirst-EARLY
osmoreceptors/ low osmolality

-hypovolemic -LATE
baroreceptors/ blood volume
*Renin-angiotensin-aldosterone system
ALDOSTERONE PRODUCTION

1)Blood flow to glomerulus drops
2)Juxtaglomerular cells secrete renin
3) renin travels in blood to liver
4)Renin - angiotensinogen to angiotensin I
5)Angiotensin I travels to lungs
6)it is converted to angiotesin II by Angiotensin Converting Enzyme (ACE)

EFFECTS
1) triggers sympathetic response
2) adrenal glands releases aldosterone
3) posterior pituitary releases ADH


Renin-releases w/low BP or osmo
=vasonstriction

Angiotensin II
=vasoconstriction/ thirst/ aldosterone release

so.........
if kindeys are not getting perfused this system is triggered and will cause BP to increase
*ALdoSTerone

where is it made
what can mimic it's effects
steriod, mineralcorticoid produced by....
adrenal glands (cortex)

Effects:
- Na retention(H20 follows) and K excretion
=increases fluid vol and B/P, decreases UO

Triggers:
-plasma acidosis (high serum K)
-increased ACTH
-low B/P and/or FVD = stretch receptors/ Renin-angiotensin system
-sympathetic response
-diurnal cycle (higher at night)

*remember it is a steroid so cortisol can have a similar effect
Calcitonin
a thyroid hormone

lowers serum Ca by inhibiting..
-osteoclasts in bones
- intestines in absorbing Ca
-kidney Ca reabsorption
-kidney Phos reabsorption

release stimulated by
-increased serum Ca
-gastrin
*ANP
Atrial natriuretic peptide

cardiac hormone found in atria cells, released when BP increases
(also when serum Na increased)

shuts OFF the renin-angiotensin-aldosterone system

-it causes vasodilation (decreased BP) and reduces fluids (increasing Na and H2O excretion)

DETAILS:
• suppresses serum renin levels
• decreases aldosterone release
• increases GFR=increases urine excretion
of Na/H20
• decreases ADH release from the posterior pituitary gland
• reduces vascular resistance by causing vasodilation
Anions

list some
negative charge

• Bicarbonate
• Chloride
• Phosphorus
cations

list some
positive charge

-remember "t"="+"

• Calcium
• Magnesium
• Potassium
• Sodium

*all cation end in "ium"
milli equivalents per liter (mEq/L),
measure of the ion’s chemical activity, or its power
how much sodium do you need a day?
1 to 2 mEq/kg/day

recommended = 2g/day
how much potassium do you need a day?
0.5 to 1 mEq/kg/day

recommended= 40mEq/day
pH

what is normal body/serum pH
calculation based on the percentage of hydrogen ions in a solution

(7.35-7.45) normal in body
acid
consist of molecules that can give up, or donate, hydrogen ions to other molecules

-more hydrogen ions
-lower pH
-AKA acidotic
-ie carbonic acid
-pH below 7

EX:
H2CO3 (carbonic acid) - H=HCO3
base
consist of molecules that can accept hydrogen ions

-has fewer hydrogen ions
-has a higher pH
-AKA as alkaline
-pH above 7
-ie bicarbonate
chemical buffers

is it effective?

how does it work/examples
-combine with xs bases or acids
-most effective defense, 1st LINE

*remember CO2 is a potential acid
CO2 + H2O =H2CO3 (carbonic acid)

The carbonic anhydrase equation AKA
the buffer system reverses the process

H2CO3 (carbonic acid) - H=HCO3(bicarb)

*works either way to keep balance
*The respiratory system (pH)
-2nd line of defense AKA
COMPENSATORY
-acts fast but don't last
-regulates blood levels of CO2
-chemoreceptors in medulla respond to changes in pH by changing respiration
*Renal system (pH)
-also 2nd line COMPENSATORY
-takes a few days but lasts and lasts
-can absorb or excrete acids/bases
-also can produce bicarbonate
*Normal Acid/Base values

pH
PO2
PCO2
HCO3
O2 sat.
pH (7.35-7.45)
PO2 (80-100mmHg) hypoxic if low
PCO2 (35-45) -acid /respiratory
HCO3 (22-26 meq) -base/metabolic
O2 sat. (93-100)


R-respiratory
O-opposite
M-metobolic
E- equal
how can you test the buffer system

(ratio)
Normal is 20 base: 1 acid

*compare HCO3 and PCO2
*CVP
what does it measure
and what is normal?
-Central venous pressure
-measured in R atrium
-pressure in thoracic vena cava, near R atrium
-reflects blood returning to heart
-often used to gage PRELOAD

-2 to 6 mm Hg (2 to 10 cm H2O)
-higher=more fluid/FVE
how do you estimate a persons CVP (central venous pressure)
-pulsations 3 or more cm above angle of Louis is abnml

with machines:
-must be ‘zeroed’ at level of R atrium
-usually taken to be level of 4th ICS , mid-axillary line while supine
-Each measurement taken at same zero position
*Hypovolemia
Loss of fluid from ANYWHERE
-V/D, bleeding, etc
3rd space shifting
-ascites, burns, etc
Diseases w/polyuria
-diabetes, particle induced diuresis

Labs:
-elevated BUN:creatinine
-elevated Hct and Hgb
-elevated serum osmolality
-elevated urine specific gravity
-normally decreased urine output w/increased concentration

TX:
-monitor I/O, daily wt
-STOP LOSS,hold diuretics/laxatives
-REPLACE fluids PO(mild)/IV (severe)
-FALL precautions

s/s
-increased HR
-decreased B/P and CVP
-weak, thready pulse
-increased RR
-orthostatic hypotension
-decreased turgor, dry MM, thirst
-cool, clammy skin
-mental confusion
-risk for shock
*Hypervolemia
cells only hold so much so it FILLS VESSELS 1st then tissues

CAUSES:
-THINK HEART 1st then renal F
-increased fluid and/or Na intake
(Alka-Seltzer, fleet enema, etc)
-low dietary protein
-prolonged steroid tx/Cushings
-hyperaldosteronism

S/S:
-distended neck/peripheral veins
-tachycardia
-increased B/P, CVP, weight
-increased urine output (unless DI)
-full, bounding pulse
-pulmonary edema
-S3 heart sound
-crackles in posterior bases
-SOB/ tachypnea
-frothy sputum (pink), cough
-dependent edema

DX:
-decreased Hct/ Hg
-decreased serum osmolality
-decreased urine osmolality
-decreased urine Na
-decreased urine specific gravity
-increased ANP, BNP, etc
-other s/s of cause (heart/renal)

TX:
-Restriction of Na and Fluids
-I&Os and daily wts
-Diuretics
-bedrest
*if a pt gains 1 kg in weight how much extra fluid is that
assuming it is all water weight?
1000ml
*Hypernatremia

causes

s/s

TX
CAUSES:
-hyperventilation
-heat stroke
-DI
-V/D, not drinking enough, etc
-feeding tube pts (still need H2O)

S/S:
-thirst
-elevated body temp
-dry MM, swollen tongue 
-hallucinations, seizures   
-anorexia , N/V

TX:
-fluids, diuretics, Na restriction
-daily wts, I&Os
*Hyponatremia

causes

s/s and tx
CAUSES:
-XS intake of plain water
-psychogenic polydipsia
-D5W (sugar and H2O)

S/S: of CEREBRAL SWELLING
-anorexia, N/V
-ABDOMINAL cramps
-HA/ seizures/ coma/ death

TX:
-Na replacement
-fluid restriction
-IV normal saline or hypertonic
*hypokalemia

causes

s/s

ECG changes

tx
below 3.5 mEq/L
severe if less then 2.5 mEq/L

CAUSES:
-Vomiting, NG suction (lots in GI)
-diuretics
-not eating, anorexia

S/S:
-muscle cramps
-muscle weakness
-arrythmias

ECG:
-prominent U waves
-PVCs
-V-tach

TX: um w/K of course
-Aldactone
why might the serum mag level NOT reflect a true measure?
-only 1/2 in free form (IONIZED)-active but unmeasurable
-30% of serum Mg binds to albumin
-if albumin low=Mg looks low
-20% binds to other stuff
*Hypomagnesemia

causes

s/s

ECG

tx
below 1.2 mEq/L

CAUSES:
-diarrhea (lots of Mg in intestines)
-alcoholism (suppresses ADH/anorexia)

s/s:not enough sedation
-muscles tight, rigid
-seizures
-stridor/laryngospasms
-dysphagia (aspiration)
-arrhythmias
-increased DTRs
-Trousseaus and Chvostek’s sign
-mind changes (crazy to depressed)

ECG:
-PVCs
-flat/inverted T wave
-depressed ST segment
-prolonged PR interval
-widened QRS

TX: mag sulfate
-check renal F if given IV
-seizure precautions
*Hypermagnesemia

causes

s/s

ECG

tx
serum mag above 2.1 mEq/L

CAUSES:
-Renal failure (excretes most)
-too much intake, antacids

S/S:
-warmth/flushing d/t vasodilation
-decreased DTRs,pulse,LOC,RR
-weak, flaccid muscle tone
-arrythmias

ECG:
-tachycardia to bradycardia
-prolonged PR interval and QRS
-peaked T waves

TX:
-calcium gluconate
-mech ventilation
-dialysis
-safety precautions
Urine specific gravity



*LEAST accurate measure of urine concentration
-measure of kidneys’ ability to excrete/conserve urine
-compared to wt of distilled water (1.000)
-can be measured at bedside
-varies inversely w/urine volume
-increased glucose/protein=falsely high
-1.010 to 1.025
BUN




*measure of renal function
made of urea (end product of protein metabolism by liver) from both muscle and dietary intake
-amino acids breakdown into ammonia which is transformed into urea than excreted in urine
-elevated in renal failure, dehydration, and hemorrhage
-10-20 mg/dL (3.6-7.2 mmol/L)
Creatinine
*better measure of renal function than BUN because it does not vary with dietary intake of protein and metabolic state
creatinine is the end product of muscle metabolism
-depends on lean body mass (individual)
-increased levels=decreased renal function, muscle damage, dehydration
-approx. 0.7 to 1.4 mg/dL
Bun to Creatinine ratio
20:1
(BUN about x20 the creatinine)
-elevated w/
-decreased renal function
-hypovolemia
Hematocrit (Hct)
-measures % of RBCs in blood

-increased values=FVD
-decreased values= FVE

-males 42% to 52%
-females 37% to 47%

normaly 3x the hemoglobin
RL

what is it often used for
what is in it
when should it NOT be given
what does the L change into
-isotonic
-often used as fluid volume expander
contains: Na, Chl, K, Ca, and………
Lactate-metabolised into bicarbonate
-not given if pH is more than 7.5
-9 cal/L
D5

calories per L

-170 cal/L
what pH levels will cause DEATH
below 6.8 or above 8.0
s/s respiratory acidosis

causes

tx
too much CO2
-mid abd incision
-narcs, sleeping pills, sedatives
-pneumothorax
-pneumonia
-COPD???

-elevated B/P and HR
-decreased heart contractibility
-HA, confused, lethargy to coma
-HYPERKALEMIA
-hypoxia=restlessness, increased HR

TX: depends on cause
-mechanical ventilation
-O2 therapy
-insulin=pushes K into cells
s/s respiratory alkolosis

causes

and tx
CAUSES:
-hyperventilation
-acute aspirin OD
S/S:
-lightheaded, faint
-peri-oral numbness
-tingling in fingers/toes
-HYPOCALCEMIA
-HYPOKALEMIA

TX:
-decrease respirations/calm/sedate
-breathe into paper bag
-again tx the cause
metabolic alkalosis

causes

s/s

tx
too many H+ (ions) lost from.....
-diuretics
-corticosteriods
-aldosteronism
-Cushing's Dz
-vomiting/suction=lose HCL

S/S:
-HYPOCALCEMIA
-HYPOKALEMIA

TX:
-Diamox (diuretic)
-IV POTASSIUM
metabolic acidosis

causes

s/s

tx
-seizures/fever
-diarrhea=lose HCO3
-renal failure
-starvation and DK, d/t ketones

S/S:
-elevated B/P, HR, and RR
-decreased heart contractibility
-lethargy to coma
-HYPERKALEMIA

TX: the cause
-IV NaBicarb
*Hyperkalemia

causes

s/s

ECG

tx
CAUSES:
-renal F (most K excreted in urine)
-use of Aldactone

S/S:
-begins w/muscle twitching
-proceeds to weakness
-then flaccid paralysis
-arrhythmias

ECG:
-tall tented T waves
-widened QRS complex
-flat or absent P waves
-bradycardia
-conduction blocks
-V-fib

TX:
-Kayexalate
-insulin =pushes it into cells
-calcium gluconate-for heart
-diuretics
- dialysis,
-IV sodium bicarbonate if acidosis
*serum Na level
135-145
*serum K level
3.5-5.5
*serum Ca level
8.5-10.5
*serum Mag level
1.2-2.1
serum Phosphate level
2.5-4.5
serum chloride level
96-108
*Hypercalcemia

causes

s/s

ECG

TX
CAUSES:
-hyperparathyroidism= XS PTH
-Thiazide diuretics
-immobilization

S/S
-Bones, brittle
-Stones (renal/biliary)
-decreased DTRs,pulse,LOC,RR
-weak, flaccid muscle tone
-arrythmias

ECG:
-shortened ST segment and QT interval
-braycardia

TX:
-Movement, weight baring
-fluids to prevent stones
-calcitonin
-steroids
- phosphate salts /Fleet enema, and other forms phosphorus
*Hypocalcemia

causes

s/s

ECG
above 10.5mg/dL

CAUSES:
-Not enough PTH
(hypoparathyroid, thyroidectomy, radical neck)

S/S:
s/s:not enough sedation
-muscles tight, rigid
-seizures
-stridor/laryngospasms
-dysphagia (aspiration)
-arrhythmias
-increased DTRs
-Trousseaus and Chvostek’s sign
-mind changes (crazy to depressed)

ECG:
-prolonged QT interval
-lengthened ST

TX:
-Vit D
-Phosphate binders
-IV Ca =must use heart monitor
*Relationship between Ca and phosphorus
Are opposite so when one goes up the other goes down
Tetany

s/s
caused by
-hypocalcemia and hypomagmesemia
-HYPERACTIVE DTR
-tingling in fingers,feet,mouth
-spasms that may be painful
*Trousseau's sign
-carpal spasm w/B/P cuff 20mmHg above systole w/n 5 minutes
*Chvostek’s sign
-twitching d/t tapping of facial nerve
ways to measure urine concentration

from least to most accurate
-specific gravity
-osmolarity
-OSMOLALITY
*concentrated makes the numbers go up............

and

dilute makes the numbers go down rule
ONLY works with:
-urine specific gravity, Na, and Hct

remember when looking at labs
serum and urine
*SIADH
-too much ADH
(too many letters=too much H2O)

-retains fluid d/t decreased diuresis
=increased urine concentration and decreased output
=decreased serum concentration and increased volume
*DI
-diabetes insipidus
D=Diuresis
-not enough ADH

-urine is dilute
-serum is concentrated
-may go into hypovolemic shock
*where is ADH found

and why is this significant
-pituitary

potential ADH problem (DI):
-craniotomy
-head injury
-sinus sx
-transphenoidal hypophysectomy
-or anything that could increase ICP
*common drugs used to tx low ADH/ DI
-Vasopressin (Pitressin)
-Desmopressin Acetate (DDAVP)
*common diuretics used
K wasting:
-Furosemide (Lasix), loop
-Hydrochlorothiazide (Bumex)

K sparing:
-Aldactone

think about this when making IV and dietary choices about K
*test tip

anytime you see assessment or evaluation look for......
presence or absence or PERTINENT (focused) s/s
*what effect does bed rest have on fluid volume
-it induces diuresis =decreasing vol
-increased fluid in thorax stimulates release of ANP
-and causes baroreceptors to trigger decreased ADH production

-this may be used to tx FVE

-may also cause FVD
-increased blood thickness, DVTs, thickness of secretions, constipation etc.........................
so PUSH FLUIDS unless in FVE
*anecdote to Magnesium
and how is it given
Calcium gluconate

IVP max rate of 1.5-2mL/min
*test tip

Mg and Ca questions, think......
muscles 1st

-too much=sedatives
-too little=not enough sedatives
*dietary sources of phosphorus
anything w/protein
*common phosphate binders and use
-Renagel, PhosLo, Os-Cal

-brings down serum phosphorus and increases serum Ca
* foods high in Mg
-spinach and kale
-mustard and turnip greens
-broccoli
-green beans
-celery
-summer squash and cucumber
-peppermint
-pumpkin/flax/sesame/sunflower
-halibut
*foods high in K
-spinach, fennel, and kale
-mustard greens
-broccoli
-brussel sprouts
-bell peppers
-cucumber
-cauliflower
-cabbage
-parsley
-lima beans
-eggplant
-halibut and tuna
-avocado, banana, kiwi, ginger
-strawberries, oranges, apricots
-cantaloupe
-tomatoes and both potatoes
* Kayexalate
used to tx what?
hyperkalemia

-exchanges Na for K in GI tract
-pt may become dehydrated
-push fluids
*Any time you give IV insulin worry about.......
-hypoglycemia
and
-hypokalemia
*major considerations w/PO and IV K
PO= give w/food to avoid GI upset

IV
-assess urine output b4 and during
(drop in output=increased retention just like w/Mg)
-always use a pump
-mix well
-DILUTE, it BURNS
parathyroid hormone
PTH=bone resorption
increases serum calcium by ..
-kidney keep Ca and Mag
-kidneys ditch phos
-osteoclasts increased
-increased absorption by GI via VitD

release stimulated by....
-decreased serum Ca
-mildly decreased serum Mag
-increased serum Phos

inhibited by....
-increased serum Ca
-severe decrease in serum Mag