High acuity fluids and electrolytes Flashcards
osmosis
movement of H20 between compartments across permeability membrane
osmolality
concentration of solute in body of water
starling forces
governs the passage exchange of water between the capillary microcirculation and the interstitial fluid
an equation that illustrates the role of hydrostatic and oncotic forces
hydrostatic pressure
pressure exerted by fluid in the interstitial or capillary space against the cell wall
arterial=high
venous=low
oncotic pressure
pressure exerted by plasma proteins in the capillary or within the interstitial space
second space edema
pitting and non-pitting edema
in the interstitial space
third space fluid
ascites
body cavities that normally don’t have fluid
isotonic solutions
closely approximates normal serum plasma osmolality
NS and LR
hypotonic solutions
shifts fluids from the intravascular compartment into intracellular compartments
FLUID INTO CELL
1/2NS, D5W
hypertonic solutions
shifting fluids from ICF and ECF into intravascular compartment (expands blood volume)
D10W, D51/2NS, 3%NS
hypernatremia causes
renal losses
hypertonic feedings (tube feeds)
increased Na intake
hyperaldosteronism
high stress & increased cortisol
diabetes insipidus
hypernatremia symptoms
FRIED SALT
flushed skin and fever
restless, irritable, anxious, confused
increased blood pressure and fluid retention
edema: peripheral and pitting
decreased urine output
skin flushed
agitation
low-grade fever
thirst
hypernatremia treatment
depends on cause (treat cause)
fluids
DI -> give ADH
reduce Na intake
tx aldosteronism
hyponatremia causes
use of diuretics
vomiting
diarrhea
diaphoresis
urination
hypovolemia
SIADH
hyponatremia symptoms
SALTLOSS
stupor/coma
anorexia, nausea, vomiting
lethargy
tendon reflexes (decreased)
limp muscles (weakness)
orthostatic hypotension
seizures/headache
stomach cramping
hyponatremia treatment
increase Na to H2O ratio
give Na
tx underlying cause
restrict fluid
normalize serum osmolality
assess volume status of patient
assess urine sodium concentration
diabetes insipidus
“water diabetes”
abnormal secretion or action of ADH
diabetes insipidus s/s
up to 20L urine/day
low specific gravity
low osmolarity
hypovolemia
increased thirst
tachycardia
hypotension
4 types of DI
central
nephrogenic
gestational
primary polydipsia
central diabetes insipidus
decreased secretion of ADH
causes: idiopathic, head trauma, pituitary tumor, neurosurgery
nephrogenic diabetes insipidus
kidney resistance to ADH
causes: lithium toxicity, renal disease, hypokalemia, pregnancy, meds
diagnostic criteria for DI
low urine osmolality
high serum osmolality
low urine specific gravity
hypernatremia
DI treatment
hormonal replacement therapy with Desmopressin or Vasopressin
DI collaborative management
frequent neuro assessments
monitor I&O hourly
monitor electrolytes
replace fluids
hormonal replacement
SIADH
increased production of ADH
increased water reabsorption in renal tubules
increased water retention and dilutional hyponatremia with a low serum osmolality
causes of SIADH
brain damage: meningitis, SAH
infective: pneumonia, lung or brain abscess
hypothyroidism
malignancy: SCLC
drugs: carbamazepine, SSRIs, amitriptyline, morphine
SIADH pathophysiology
increased production/release of ADH
increased water reabsorption/retention
water intoxication
SIADH s/s
oliguria (<400mL/24hr) in absence of hypovolemia
hyponatremia
high urine specific gravity (>1.02)
SIADH lab manifestations
low serum Na (<130)
low serum osmolality (<280)
high urine osmolality (>500)
high urine Na (>20)
SIADH collaborative interventions
frequent neuro assessment
water restriction
seizure precautions
high sodium diet
NS IV or hypertonic saline
demeclocycline (derivative of tetracycline)
rhabdomyolysis definition
rapid release of cellular contents from damaged skeletal muscle cells
rhabdomyolysis causes
muscle injury: trauma, burns, electrocution, immobilization, metabolic disorders, DKA, hyponatremia, hypokalemia, hypophosphatemia, ischemia, compression, vascular injury, SCD
meds/illicit drugs
increased muscular activity: sport, seizures, status asthmaticus, infections, inflammatory myopathies, hypo/hyperthermia, idiopathic
s/s of rhabdomyolysis
myoglobinuria (brown urine)
hyperuricemia
hyperkalemia
hyperphosphatemia
hypocalcemia -> cardiac arrythmias
elevated Creatinine kinase
rhabdomyolysis complications
AKI
compartment syndrome
DIC
MODS
rhabdo collaborative management
alkalinization of urine
correct electrolyte imbalances (reverse acidosis)
IV hydration and diuresis (NPO status)
fasciotomy
dialysis
tumor lysis syndrome definition
rapid tumor cell death resulting from cancer therapy causing rapid release of intracellular contents
highest risk tumor types for tumor lysis syndrome
non-hodgkins lymphoma
acute leukemias
chronic lymphoblastic leukemia
solid tumors
pathophysiology of tumor lysis syndrome
complex series of events causing spilling of intracellular contents from tumor cells,
an inability of the kidneys to excrete and maintain normal serum levels
s/s of tumor lysis syndrome
hyperuricemia
hyperphosphatemia
hypotension
hyperkalemia
hypocalcemia -> cardiac arrythmia and arrest
fluid overload, weight gain, edema -> respiratory failure
anuria
oliguria
weakness
lethargy
cramping
tetany
renal insufficiency
flank pain
N/V/D
s/s of hyperuricemia
N/V
azotemia
oliguria/anuria
decreased urine pH
uric acid crystals found in urinalysis
hyperkalemia s/s
EKG changes: flat P, wide QRS, high T
weakness
twitching
hyperactive bowel sounds
nausea
diarrhea
hyperphosphatemia s/s
hypocalcemia
joint/muscle pain
renal failure
hypertension
edema
hypocalcemia s/s
cramping
tetany
Chvostek’s sign: muscle twitch on cheek
Trousseau’s sign: arterial blood flow occlusion with fingers extending
EKG changes: prolonged QT
tumor lysis syndrome collaborative management
administer allopurinol
alkalinization or urine
correct electrolyte imbalance
aggressive hydration starting prior to chemo
dialysis
hepatorenal syndrome
occurrence of renal failure in a patient with advanced liver disease in the absence of an identifiable cause of renal failure
HRS etiology
serious complication of liver cirrhosis with poor prognosis
portal vein HTN fluids back up into abdomen
2 types of HRS
type 1: decreased systemic circulation (BP)
type 2: severe ascites, refractory to diuresis
HRS pathophysiology
portal hypertension -> splanchnic vasodilation -> decreased effect circulatory volume -> RAAS activation -> renal vasoconstriction -> HRS
hepatic-related ascites
liver cirrhosis is most common cause
ascites is caused by a combo of increased hydrostatic pressure in liver veins (Portal HTN) and decrease in colloid osmotic pressure
HRS s/s
type 1: rapid, progressive
type 2: chronic, slowly progressive
general:
liver failure w/ increased LFTs
oliguria
decreased serum and urine Na
increased BUN and Cr
decreased GFR
HRS collaborative management
fluid restriction
CRRT
pharm: midodrine, octreotide, albumin
surgical: liver transplant, transjugular intrahepatic portosystemic (TIPS) shunt
NANDAs
excess fluid volume
deficient fluid volume
electrolyte imbalance
impaired liver function
