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complications of fluid overload/hypervolemia
pulmonary edema
arrhythmias bc of dilated electrolytes and Hgb
third spacing bc of excessive hydrostatic pressure → pressure on vital organs
heart failure
portal HTN
esophageal varices
aneurysm
stroke
complications of fluid deficit/hypovolemia
hypoperfusion
multiorgan dysfunction syndrome (MODS)
falls
ortho hypotension
weakness
altered MS
concentrated electrolyte levels
cues of fluid imbalance
medical record
age, sex, obesity
PMHx (CKD, CHF, cirrhosis vs hypermetabolic and wound)
meds
labs
provider orders and context
LDA’s
V.S
key assessment findings of fluid imbalance
weight change >1kg gain/loss
urine output of <30 mL/hr or 0.5 mL/kg/hr discrepancy
I/O of >500-1000mL discrepancy
dry skin
xerostomia
pulse quality
venous distention
dyspnea
edema
risk factors for dehydration
elderly females
individuals with high body fat content bc of decreased muscle mass to store water
older adults have reduced thirst reflex, renal function, and ability to concentrate urine
difficult to assess fluid status bc of lower skin elasticity and baseline skin turgor
hypermetabolic and wound conditions
NPO status
environment that causes excess sweating
labs: elevated Hct, sodium, and increased urine concentration
diuretics
risk factors for excess fluid
CKD
HF
cirrhosis
anticholinergics
liver harming drugs
s/s of hypovolemia/dehydration
dry skin/mucous membranes
poor skin turgor
weak pulses
weight loss of >1kg indicates a 1L fluid loss
s/s of hypervolemia/excess fluid retention
JVD
adventitious heart sounds
third spacing fluid → edema, crackles, ascites
weight gain of >1kg indicates a 1L fluid gain
what controls INPUT of fluid balance?
hydration (IV and PO)
foods
other sources (ex: enemas, irrigations)
what controls OUTPUT of fluid balance?
urine (diuresis)
bowels (enemesis and stool)
drains
insensible water loss (about 0.5-1L/D)
what controls FLUID COMPARTMENTS/DISTRIBUTION of fluid balance?
intracellular
extracellular
vascular
interstitial
other
conditions that interfere decreased UO
AKI oliguric phase
CKD
obstructive urinary conditions
hormones (hyperaldosteronism, SIADH, HF, BNP-induced CKD)
conditions that interfere with increased output
AKI diuresis phase
GI issues
hypermetabolic state
hyperventilation
wounds, burns, bleeding
hypoaldosteronism
DI
factors that interfere with UO
AKI acute oliguric phase (first 48h of recovery)
CKD can interfere with UO bc of inability to excrete sodium and water or can increase UO bc inability to reabsorb sodium and water
hormones
aldosterone (renal cortex function)
antidiuretic hormone
hypercortisolism
hyperaldosteronism
excess RAAS
excess ADH (SIADH)
HF → increased release of natriuretic peptides from heart cells which initially causes natriuresis → increased sodium and water excretion via kidneys → eventually become into renal damage and decreased UO
factors that increase UO
AKI diuresis phase
GI issues
metabolism
fever
extreme stress
thyroid crisis (increases water loss)
high RR and distress or ventilation bc of increased water loss
wounds/burns
bleeding
hormonal: renal failure, adrenal insufficiency → hypoaldosteronism, diabetes insipidus
what is syndrome of inappropriate diuretic hormone (SIADH)?
condition where the body produces or releases too much antidiuretic hormone (ADH), leading to excessive water retention and low blood sodium levels (hyponatremia)
diabetes insipidus
condition that causes excessive thirst and urination due to a deficiency or resistance to antidiuretic hormone (ADH)
fluid compartments in extracellular spaces
vascular
interstitial (brain interstitial fluid/synovial/peritoneal/pleural compartments)
bone
lymph
connective tissues
where should most body fluid be?
intracellular and vascular spaces to promote cellular function and perfusion
fluid being where starts causing issues for a patient
stuck in limb or in third spacing to the interstitial
causes pulmonary edema, ascites, etc
conditions that cause third spacing
decreased blood osmolarity
albumin bc of liver failure
sodium
glucose/insulin levels bc of diabetes
increased blood hydrostatic pressure (HTN)
porous membranes/leaky capillaries bc of inflammation
how can someone be fluid overloaded but hypovolemic?
insufficient vascular osmolarity d/t hypoalbuminemia or leaky capillaries
albumin
protein in blood made by the liver that is responsible for pulling in and holding water in the bloodstream to maintain adequate vascular volume and blood circulation
how can cirrhosis/liver disease cause fluid overload but hypovolemia at the same time?
liver does not make enough albumin
insufficient pulling and water leaks into the interstitial spaces
leads to a perpetuating cycle of fluid retention bc hypovolemia leads to less urinary excretion → AKI → impaired ability to create urine
s/s
ascites
extremity pitting edema
pleural effusions
less vascular volume (hypovolemia)
how can someone be fluid overloaded but cellularly dehydrated?
sodium is more abundant in the ECF (particularly in the interstitial) than ICF and water follows sodium
intake of high salt → water shifts outside of cell into interstitial space → cellular dehydration while overall body fluid continues to build up in ECF compartments
management for hypovolemia
rehydrate to maintain perfusion (PO/enteral pref first)
prevent falls
monitor at least pulse quality and urine output q2h
strict I/O’s
q8hr daily weights
address underlying cause (antiemetics, antidiarrheals, ABX, antipyretics, desmopressin for diabetes insipidus)
potentially albumin infusion if pt has hypovolemia with excess interstitial fluid
hypotonic IV fluids
0.3% NaCl
0.45% NaCl
D5W*
indications: cellular dehydration
isotonic IV fluids
crystalloids (NS, LR)
indications: ICF/ECF dehydration
hypertonic IV fluids
colloids
albumin
10-15% D5W
3% NaCl
NaHCO3 5%
D5W + 0.9% NaCl
indications
hypovolemic but fluid overloaded so it draws fluid into vascular space
D5W
starts isotonic but goes hypotonic once body metabolizes the sugar
complications of infusions
infiltration
hematoma
embolism
thrombosis/endarteritis
types of infiltration
phlebitis
thrombophlebitis
phlebitis
inflammation of vein
thrombophlebitis
condition where a blood clot (thrombus) forms in a vein and causes inflammation
management of infiltration
discontinue IV
compress
sometimes extremity elevation
restart IV proximal
hematoma
localized collection of blood outside of a blood vessel
hematoma management
discontinue IV
pressure dressing
cool compress for 24 hours then warm compress
clot management
give alteplase
circulatory overload management
SLOW infusion
assess V.S and labs
Notify HCP
hypervolemia management
prevent falls
monitor cardiorespiratory complications
pulmonary edema
HF
arrhythmias
impaired skin integrity
maintain skin integrity (assess and reposition q2h)
give diuretics (loop, thiazide, potassium sparing, osmotic)
strict I/O’s
daily weights at same time each day (best before breaky and w same amount of clothing and linen - upon admission ensure bed is zero’d with standard linen count)
PRN HF agents (ARBs, BBs, inotropics like dig)
give vasopressin antagonist in cases of hypervolemic hyponatraeemia (ex: conivaptan/tolvaptan)
restrict fluid and sodium intake
loop and thiazide diuretics
natriuretic diuretics blocking reabsorption of NaCl and passive water reabsorption
thiazides are slower and weaker and Cl’d in renal impairment bc its mechanism depends on kidneys ability to excrete sodium and chloride in first place
loop diuretics work in renal disease because they work even when GFR is low
thiazide SE similar to those of loop diuretics except ototoxicity
ex of loop: furosemide, bumetadine, torsemide
potassium sparing diuretics
often contraindicated in cases of renal failure
ex: spirinolactone
mannitol
freely passes through glomerulus into nephron and minimally reabsorbed
with osmotic pressure it draws nephron for diuresis
many s/s of electrolyte imbalance share these SE…
anorexia
N/V
numbness
tingling
acidosis and electrolyte levels
associated with high electrolyte levels
less excitable tissue
acid is WEAKER, LOOSER, and SLOWER
alkalosis and electrolyte levels
associated with low electrolyte levels
alkaline is HYPER, TENSER, FASTER, IRRITABLE
normal potassium levels
3.5-5.0
hypokalemia causes
excessive diuresis/excretion
loop/thiazide diuretics
mineralocorticoid steroids
insulin
NG suctioning
abd surgery
liver/renal disease
too much water intake
K+ depletion
dilution
mass transfusion
hypokalemia s/s
weak CV
digoxin potentiation
arrhythmias
variable HR
weak thready pulses
inverted T waves
depressed ST segment
reduced tissue excitability
hypokalemia management
PO/enterally best
if giving supplement give it with food to decrease irritation and increase absorption
foods: raisins, bananas, apricots, oranges, beans, potatoes, carrots, celery
if IV infusion do 10-20 mEq/hr
monitor cardiac
correct K+ before pH
correct Mg+ before K+
why do you correct K+ before pH?
hypokalemia contributes to alkalosis so correcting potassium will help correct pH
why do you correct Mg+ before K+?
Mg+ helps correct the kidneys so they hold onto K+ better
hyperkalemia causes
renal failure
mass transfusion
burns
fractures
severe infection
K+ sparing diuretics
ACE’s
lysis of stored and irradiated RBC’s
hyperkalemia s/s
slower CV conduction
peaked T waves
bradycardia/heart block
widened QRS
prolonged PR
general tissue excitability is increased
muscle twitching
hyperkalemia management
C.A.B.I.G.K.Drop
administer glucose before the insulin to avoid causing the pt to go into hypoglycemia
C.A.B.I.G.K.Drop meaning
a treatment for hyperkalemia in emergency situations
calcium
albuterol
bicarb
insulin and glucose
kayexalate
dialysis, diuretics, diarrheal agents, dietary restriction
normal calcium range
9-10.5
hypocalcemia causes
hypoparathyroidism/post-op
vitamin D deficiency
renal failure
pancreatitis
mass transfusion
how does mass transfusion cause hypocalcemia?
mass transfusion of citrate containing pRBC’s causes citrate to bind with calcium to prevent clotting
hypocalcemia s/s
chvostek sign
trousseaus sign
tetany
seizures
hyperactive reflexes
bronchospasm
bleeding
chvostek sign
twitch of the facial muscles that occurs when gently tapping an individual's cheek, just in front of the ear
trousseaus sign
when inflating BP cuff, the hand will twitch/goose hand
hypocalcemia management
PO calcium
calcitriol with vitamin D
chloride with vitamin c for max absorption
seizure precautions
maintain airway
regular exercise
phosphate binders
push Mg+ if necessary
hypercalcemia causes
malignancy
hyperparathyroidism
prolonged immobilization
hypercalcemia s/s
lack of coordination
ALOC
dyrhythmias
nephrolithiasis
decreases excitability of tissues overall
hypercalcemia manegement
important to HYDRATE bc risk for kidney stones (NS, ½ NS IV, PO)
loop diuretics
calcitonin
mobilization
dietary restriction
antiacid restriction
normal sodium levels
135-145
hyponatremia causes
excessive diuresis/excretion
sodium depletion
dilution
SIADH
HF
hyponatremia s/s
neuro: seizures, ALOC, coma, death
GI: n/v/d, cramping
why does hyponatremia have serious neuro symptoms?
hyponatremia causes cerebral edema → coma → death
hyponatremia management
correct slowly IV
correct rapidly PO
isotonic IVF
H2O restriction
I/O
daily weights
hypernatremia causes
prerenal failure
hypertonic tube feedings
diabetes insipidus
hyperosmolar hyperglycemic state (HHS)
dehydration
drugs (ASA, citric acid, NaHCO3)
diabetes insipidus
cause of insufficient ADH which leads to polyuria
neurogenic: not enough ADH released
nephrogenic: renal tubules not able to use ADH
s/s
high serum osmolality
polyuria (>200 mL/hr x 2 hr)
polydipsia
s/s of dehydration
treatment
hydration (ex: .45% NaCl
ADH
hydrochlorothiazide
hypernatremia s/s
thirst
febrile
dry
swollen
s/s of dehydration
hypernatremia management
hypotonic solutions only in extreme situations
decrease PO sodium
daily weights
normal magnesium levels
1.5-2.5
magnesium is like…
like a sedative/muscle relaxant
hypomagnesemia causes
alcoholism
other K+ or Na+ causes
hypomagnesemia s/s
coronary spasm (torsades)
hypokalemia
twitching
tremors
hypomagnesemia management
PO or IV magnesiumSO4 (can push if needed)
cardiac and seizure precautions
assess airway
BP
reflexes
K+ and Ca+
hypermagnesemia causes
renal failure
excess Mg from antacids or laxatives
acidosis
DKA
hypermagnesemia s/s
drowsiness
depressed
hypermagnesemia management
diuresis with fluid replacement
support ABC’s
IV calcium gluconate