Exam 1 Flashcards
Dosing body weight DBW
IBW + 0.4 ( wt-IBW)
Nutritional Body Weight NBW
IBW + 0.25 ( wt- IBW)
sensible fluid losses
urination
defecation
wounds
insensible fluid loss
skin/ sweat
lungs/respiration
ADH does what to fluids
reduces diuresis and inc water retention
RAAS does to fluids
renin secretion
Na/h20 regukation
active transport sodium
INC water retention
ANP does to fluids
DEC ADH release
conuteracts RAAS
electrolytes found in urine
Na and K
electrolytes found in NG output
Na/ Cl
small trace K
electrolytes found in GI fluid
NA
electrolytes found in pancreas
Na/Cl/ Hco3
electrolytes found in sweat
na/cl
faint trace K
electrolytes found in diarrhea
na/cl/k/hco3
isontonic tonicity
275 to 290 mosm/L
hypotonic tonicity value
<275 mosm/L
what do we experience w/ hypo tonicity
- less concentrated fluid than extracellular fluid
- fluid will move into cell
what do we experience w/ hyper tonicity
- more concentrated than extracellular fluid
- fluid pulled from the cells into the bloodstream
this is the measure of solute concentration
osmolarity
eqn of total osmolarity
Osmolarity of IV sln + Osmolarity of added electrolytes
clinical estimation of adult daily fluid requirement
30-40 ml/Kg/day
Ideal fluid has most importantly?
cost-effective
predictable effects
sustained INC in intravascular volume
normal sodium range
135-145
Normal saline Vs balanced salts
balanced salts = way to go
Are used to INC plasma oncotic pressure and
moves fluid from interstitual-> intravascular
colloid solutions
These solutions maintain perfusion to organs
colloids
albumin indications
edema/ volume expansion shock burn ARDS cardiopulm bypass intraop fluid repletion *supportive / symptomatic tx
adverse effects of albumin
hypervolemia
azoemia ( renal failure)
colloids are good for patients low on _____
protein
two factors that determine synthetic colloid type
substitution ratio
molecular weight
higher SR ( sub ration) the more?
prolonged intravascular expansion
safety concerns for synthetic colloids
( black box) sepsis/ renal failure
use with caution
1 unit RBC’s = ? mLs
230-350mL
-will INC Hb by 1g/dL
normL Hb range
12
-low <7-8
indications for blood
- acute blood loss
- inadeuate resusictaion from fluids alone
- preop
- low Hb
tachycardia, hypotension, weak pulses,dec urine output and BUN/SCr ratio<20 are signs of
dehydration
Goals of Fluid Resuscitation: ANCAR
achieve: stability/normal volume/perfussion
normalize: cell metabolism/acid-base
compensate: for fluid shifts
avoid: inflam cascade/reperfusion injury
reduce: vasopressors/edema
as acidosis resides we expect lactate levels to?
dec
goal of shock fluid resucitation
perfusion throughout patient w/ fluids and vassopressor support
shock fluid resucitation goals:
CVP-
MAP-
UOP-
CVP: 8-12
MAP: 65
UOP: 0.5
Osm calculation
(2 X Na) + (BUN/2.8) + ( Glucose/18)
When does OG exist and what does it say
if the difference between measured and calculated osmolality > 15
-it identifies the presence of additional particles
elevated lipids and proteins
increased plasma volume–> dilution
experience OG
psuedohyponatremia
This sodium state is most likely seen with an increase of blood glucose
hypertonic hyponatremia
For every INC of BG over 100mg/dl… what happens to sodium serum levels
drop 1.6meq/L for ea 100mg/dL
Corrected sodium eqn
Na serum +1.6[( BG-100)/100]
Causes of hypovol, hypoton,hyponatremia
Renal (urine Na> 20meq) -diuretics -adrenal insufficiency -salt losing nephtopathy, cerebral salt wasting Non renal (urine Na< 20meq) -bloodloss/hemorrhage -skin losses -GI losses
Causes of isovol, hypoton, hyponatremia
- adrenal insufficency ( glucocorticoid def)
- hypothyroidism
- pscychogenic polydipsia
- SIADH (most common cause)
signs of SIADH
urine Osm > 100mOsm/kg
Urine Na generally > 20-30mEq/L
-restric free water 1st line
causes SIADH
tumors, CNS disorders DRUGS -Antineoplastics -Antipschotics -Carbamzepine -SSRIs -Nicotine -NSAIDs -Oxycontin -TCa's
Clinical settings that hypervol, hypoton, hyponatremia can be seen
- cirrhosis
- heart failure
- kidney failure
- nephrotic syndrome
This range of sodium is typical to asymptomatic hyponatremia
> 125mEq/L
Most common goal is to avoid a rise in serum Na that is greater than??
0.5mEq/L/Hr
or
8-12mEq/L/Day
hypovolemic tx
symptomatic: Hypertonic 3% NaCl
asymptomatic: isotonic NaCl
isovolemic tx
symptomatic: Furosemide and 3%NaCl
asymptomatic: water restriction and isotonic NaCl
hypervolemic tx
symptomatic: Furosemide and judiciously 3%NaCl
asymptomatic: fureosemide
Rapid infusions of 3% NaCl @ 1-2 ml/kg/hr over 2-3 hrs only in what pt population?
pts with coma or sz
How do you IN sodium in a pt w/ acute symptomatic hyponatremia
MAX: 8-12 mEq/L/ first 24hrs or 1-2mEq/L/hr good short term goal is 120meq/L use 3% Hypertonic NaCl: 1/2 in first 24hrs, then rest 24-72 hours
What do Arginine Vasopressin V2/V1A receptor antagonists do?
promote excretion of free water
- no loss electrolytes
- INC urine output
- DEC urine osmolarity
- normalize Na+ levels
Arginine Vasopressin V2/V1A receptor antagonists are Vaptans and come in 2 what most common forms?
Conivaptan- IV
Tolvaptan- PO
Conivaptan treats what?
severe euvolemic and hypervolemic symptomatic hyponatremia
Tolvaptan treats what?
Asymptomatic euvolemic and hypervolemic hyponatremia
Vaptan contraindications
hypovolemic hyponat
no sense of thirst
anuria
CYP3A4 inhibitors
monitoring measures for pts w/ sypmtomatic hyponatremia
- monitored in ICU or highly monitored unit
- serial exams of heart, lungs, neuro status several times over first 12 hours
- serum Na q2-4 hours until asymptomatic
- serial Na q4-8 hours until WNL
hypernatremia is always associated w/ what tonicity
hyper
-loss of water thirst response
hypervol hypernatremia is assoc w/ ?
hypertonic fluid use
Steps to correcting hypovolemic hypernat
1) restore hemodynamic w/ NS
2) Calculate free water deficit
Parameters for replacing free water
D5W continuously or enteral feeding tube
match ins and outs
dont correct too quickly
give 1/2 deficit over 24 hours and rest over next 48
goal of Na decrease in hypernatremia
0.5ml mEq/L/hr decrease in Na serum
hyperntremia monitoring parameters
Serum Na and fluid status
-check every 3-6 hrs until symptoms resolve ( then q 6-12 hours)
I/O q 8-12 hours
overall fluid balance
What kind of sodium balance does diabetes insipidus create
isovolemic hypernatremia
tx of isovolemic hypernatremia
Desmopressin
Vasopressin
Normal range of K
3.5-5mEq/L
factors affecting Potassium lvls
Na/K pump -insulin -glucagon -catecholamines -aldosterone kidneys arterial pH/ acid base status
Hypokalemia causes
- diuretic loss
- beta agonist meds
- NG drainage–> metabolic alkalosis
- Diarrhea
- Mag depletion
Hypokalemia presentation
- nonspecific/ highly variable
- weakness or muscle wkness
- N/V
- Change in cardiac fxn or rythym ( higher risk pt)
- cramping
hypokalemia tx
serum lvl 3-3.4 -tx debatable, give PO K for cardiac risk pt serum lvl <3mEq/L -ALWAYS TX -PO if asymptomatic or IV for sx -also correct Mg deficit if present
Correction of K in hypokalemia
for every 10meQ of K given, you INC the Serum Na by 0.1mEq/L
serum lvls of severe hypokalemia and symptoms that warrant an IV
<2.5 or 3 meq
ECG or muscle spasms, unable to tolerate PO
severe hyperkalemia
> 7
hyperkalemia is what serum lvl
> 5.5
clinical presentation of hyperkalemia
peaked T wave/ flattened T wave
cardiac arrthymias
VF or asystole > 9mEq/L
Severe Hyperkalemia goals of therapy
antagonize memb actions
DEC extra cell K
remove K from the body
what two medications used to treat Hyperkalemia must go hand in hand and why
D5W and insulin because insulin draws back the K into the cell
Normal level of magnesium
1.5-2.5 mg/dL
Lvls are regulated by the kidneys and related to Ca 2+ and K+ metabolism
Mg2+
Usually associated w/ disorders of GI tract or kidneys
Diarrhea/ Dec intestinal absorp
malnutrition
drugs or alcohol cause
hypormagnesemia
Common drugs that cause hypomagnesemia
amphotericin
aminoglycosides
diuretics
cyclosporine
clinical presentaions of hypomagnesemia
- assoc w/ hypocalcemia and hypokalemia
- cardio arrthymias, tetany
- neuromusc: ataxia/ sz
- CNS: lethargy, confusion
causes of hypermagnesmia
- rare
- renal failure
- excessive laxatives
Clinical presentations of hypermagnesemia
- mg2+ >4
- neuromuscular: deep tendon reflex loss, somnolence, resp muscle paresis
- Cardio: hypoTN, arrthymias, heart block
hypermagnesemia tx
CaCl or furosemide
or supportive care
-for renal dysfxn: diuresis or hemodialysis
Normal lvls Calcium
8.5-10.5 mg/dL
low calcium causes
large blood V products mag deficiency post-op hypoparathyroid Vit D deficiency meds
Parasthesis, muscle cramps, tetany, depression, anxiety, sz, hairloss, eczema, brittle nails, hypotension, bradycardia, arrthymias are all clinical presentations of what?
Hypocalcemia
usual admin rate of calcium is??
1gm of calcium/ hr
Important for hypocalcemia tx
gluconate preferred for PIV
do not add Ca to bicarb or phosphate
give Vitamin D supplementation
Three main mech of hypercalcemia
INC bone reabsorp
INC GI absorp
DEC elimination via kidneys
Hypercalcemia clinical presentation
typically asymptomatic ( esp <13mg/dL anorexia, constipation, polyuria or dipsia, nocturia, coma arrthymias, metastic calcification, nephrolithiasis
Tx for hypercalcemia
volume expansion/ loop diuretics
calcitonin
bisphosphonates
glucocorticoids
Normal levels of Phosphorous
2.5-4.5mg/dL
clinical hypophosp presentations
sz, coma, paresthesias, hemolysis, myalgia, dysphagia, osteopenia, cardiomyopathy, dec contract, acute resp, resp muscle fatigue
hyperphos causes
renal failure/ insufficiency
hypoparathyroid
excessive intake
clinical presentation of hyperphos
soft tissue calc
hyperphos tx
IV calcium for severe
normal physiological pH range
7.35-7.45
most carbonic acid in the plasma is in the form of?
carbon dioxide
normal paCO2 range
35-45 mmHg (think 40)
normal HCO3 range
22-26 mEq (think 24)
Normal PaO2 range
95-100 mmHg
normal SaO2 range
> 95%
Dec CO, INC PVR and arrthymias and imparement of contractility are signs of
acidemia cardiac consequences
insulin resistance, inhibition of anaerobic glycolysis and hyperkalemia are signs of?
metabolic consequences of acidosis
other acidosis consequences
coma, alt mental status, dec resp muscle strength, hypervent, dyspnea
cardio consequences of alkalemia
dec coronary flow
arteriolar constriction
dec anginal threshold
arrthymias
DEC K+, Ca, and mag Over stimulation of anerobic glycolysis Dec cerebral blood flow sz DEC respirations
consequence of alkalosis
acid- base first line of defense
extra/ intracell buffering system
common buffers include
bicarb/carbonic acid phosphate and proteins
acidity can be controlled extracellularly by?
HCO3 or pCO2
two main fxns of the kidneys
- reabsorb filtered HCO3
- excrete H+ ions released from nonvolatile acids
4000-45000 mEq of HCO3 re filtered daily through?
loop of Henry
where does bicarb reabsorption take place
proximal tubule
where can we find carbonic anhydrase
RBC, brush borders of renal tubular cells, and other tissues
in case of carbonic anhydrase inhibitors
- result in urinary bicarb losses due to DEC entry of H2O and CO2
- metabolic acidosis occurs w/ increase bicarb loss
H+ excretion takes place primarily in the ?
distal tubule
50 % of net acid excretion comes from this route
distal tubular H secretion
H+ is transported back to tubular lumen by?
ATPase
Lungs are very important in ventilatroy regulation because?
rapid onset and Large capacity
When chemoreceptors detect an INC in PaCO2 what happens
INC in rate and depth of ventilation
Peripheral chemoreceptors are activated by?
arterial acidosis, hypercapnia, hypoxia
Central chemoreceptors in medulla are activated by?
CSF acidosis
Hepatic regulation of acid base
- new mech learning more about
- ox of proteins= HCO3 and NH4
- diminished hepatic urea synthesis can cause metabolic alkalosis
- a change in the urea cycle will affect HCO3 pool
Meta Acid primary change
DEC HCO3
Meta Alka primary change
INC HCO3
Resp Acid primary change
INC PaCO2
Resp Alka primary change
DEC PaCO2
Meta Acid compensation
DEC PaCO2
Meta Alkalosis compensation
INC PaCO2
Resp Acid compensation
INC HCO3
Resp Alka compensation
DEC HCO3
PCO2 should fall by 1-1.5 times the fall in plasma HCO3
metabolic acidosis
PCO2 should INC by 0.4-0.6 times the rise in plasma HCO3
metabolic alkalosis
plasma HCO3 should rise by 0.4 times the INC in PCO2 + or - 4
chronic resp acidosis
plasma HCO3 should rise by 0.1 times the increase in PCO2 + or - 3
acute resp acidosis
Plasma HCO3 should fall 0.1-0.3 times the decrease in PCO2 but not usually less than 18mEq/L
acute resp alkalosis
Plasma HCO3 should fall by 0.2- 0.5 times the dec in PCO2 but not usually less than 14 mEq/L
chronic resp alkalosis
these provide water and or sodium
maintain osmotic gradient between intravascular and extravascular
“workhorses”
crystalloids
used for intravascular fluid replacement
- resucitation, hypotension, septic shock
Sodium/ or chloride replacement
Normal saline
maintenance fluid
0.5 NS
used for replacement of blood loss
approximates human plasma
used for recsusitaion
Lactated ringers
used for free water replacement
NOT a resuscitative fluid
not a maintenance fluid by itself
dextrose
normal anion gap values
3-11 mEq
a loss of plasma bicarb is rplaced with CL
non-anion gap acidosis
delta gap
differences between patients anion gap and the normal anion gap
causes of non anion gap acidosis
gastrobicarb loss renal bicarb losses reduced renal H+ excretion - Type I RTA -Type IV RTA -Chronic renal failure Acid and chloride admin
shock drugs/ toxins seizures leukemia hapatic/ renal failure diabetes mellitus malnutrition rhabdomyloysis are all potential cases of
lactic acidosis
sx of lactic acidosis
kussmaul respiratios periph vasodialationcausing tachycardia hyperkalemia lethargy coma N/V bone demineralization
lactic acidosis acute tx
underlying cause
bicarb therapy
-use if pH < 7.10-7.15
Bicarb dosing eqn - need to know
- use for lactic acidosis
[ 0.5L/Kg (IBW) ] X ( desired HCO3- actual HCO3)
Bicarb therapy parameters
- use 12 as desired
- give 1/3 or 1/2 the calculated dose
- Cardiac arrest : 1mEq/Kg
- Supplement K if needed
hazrds of bicarb therapy
over alkanization -left shift in oxgen-Hb saturation curve hypernatremia/ hyperosmolality CSF acidosis electrolyte shift
flow of potassium in acid base disorders
in acidosis K moves extracellularly and is excreted. When bicarb therapy is used to treat acidosis, K will move back intracellularly ( more severe hypokalemia
chronic bicarb therapy for chronics metabolic acidosis
avg dose 1-3 mEq/kg/day
how does tromethamine work
combines with H from H2CO3 to form bicarb
adverse affects of tromethanmine
hyperkalemia, hypoglycemia, hypocalemia, impaired coagulation
three main mechanisma in which a rise of Bicarb would occur
loss of acid from GI tract
admin of too much bicarb/ precursor
contraction alkalosis
-loss of Cl rich and HCO3 poor fluid
volume and chloride depletion may contribute to alkalosis due to?
- Dec in arterial blood volume
- Dec ability of kidneys to excrete bicarb
- w/ volume depletion, capacity of proximal tubule to reabsorb HCO3 increases
main cause of metabolic alkalosis is
saline responsive alkalosis
with aldosterone INC we see?
Na reabsorption
inc H secretion—-> HCO3 reabsorption
inc K secretion
Diuretic therapy’s causes of saline responsive alkalosis
- extracellular volume expansion ( due to Nacl/ water secretion)
- INC distal tubule Na reabsorp/ H and K secretion ( aldosterone
- intracellular movement of H ( response to hypokalemia)
- Hypochloremic state
Three main causes of saline responsive alkalosis
Vominting/ NG
Diuretics
exogenous HCO3 admin/ blood transfusion
Why there is a maintenance of an alkaline environment in saline responsive alkalosis
- reduced GFR
- enhanced proximal tubular HCO reabsorp
- effects of hypokalemia
in terms of hypokalemia; when less K, H is scereted while Na is_______
reabsorbed
difference between saline responsive and resistant alkalosis
no chloride depletion or an inability to absorb CL in resistant
causes of saline resistant alkalosis
INC mineralcorticoid activity
hypokalemia
renal tubular chloirde wasting
INC ammoniagenesis can be causes by a low level of
potassium
due to an INC in H secretion
muscle cramps, weakness, dizziness, myocardial supression, mental confusion, CV collapses are symptoms of
saline resistant alkalosis
When would you use carbonic annhydrase inhibitors
pts that are fluid restricted or cant have excess sodium
carbonic annh inhibitor dosing
250-375 mg once/ twice daily
Therapies for persistent metabolic alkalosis
HCl
ammonium chloride
arginine monohyrdrochloride
