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IV fluids
crystalloids and colloids
crystalloids
ex: sodium chloride, dextrose, lactated ringers
Uses: dehydration, fluid maintenance, electrolyte imbalances
Described based on: Isotonic, Hypotonic, Hypertonic
distributes faster than colloids
Isotonic Fluid Names
0.9% NaCl
Lactated RIngers
Dextrose 5% and water D5W
0.9% NaCl “normal saline”
sodium chloride
uses: maintenance fluids, flush IV, give with blood, hypotension and shock
contraindications: only fluid you give blood with
Lactated Ringers LR
sodium chloride, potassium, calcium, lactate
uses: maintenance fluids, hypotension and shock
Dextrose 5% and water D5W
free water, dextrose, 1L= 17- cal
uses: maintenance fluids and provides some carbs
contraindication: increased blood glucose and no bolus
Hypotonic Fluid
0.4% NaCl “half normal saline”
uses: maintenance fluid and for hypernatremia
contraindications: monitoring neur
0.225% NaCl “ quarter normal saline”
uses: severe symptomatic hypernatremia
contraindications: monitoring neuro
Hypertonic Fluids
3% NaCl
uses: severe symptomatic hyponatreamia
contraindications: risk of demyelination syndrome and monitoring BP and lung
dextrose 5% and 0.9% NaCl
uses: maintenance fluid with hyponatremia
contraindication: monitoring Bp and lungs
water balance basics
more fat present in body= less total water content
women have more body fat
& of body water
preterrn and neonates: >70%
adults: 50-60%
older adults: 45-50%
Colloids
large molecules— stay in vascular space
increase osmotic pressure
ex: plasma, blood, albumin
dextran= synthetic form
use: treat conditions that require plasma volume expansion (shock and burns)
less livekly to cause edema and have a longer duration of action
movement of moleules and fluids
diffusion:
molecules, high to low , no energy uses
facilitated diffusion
requires carrier to move molecules
osmosis
fluid, across permeable membrane, low to high concentration until equal
active transport
molecules against gradient, low to high concentration, requires ATP energy
Osmolality
“concentration”
normal plasma: 280-295 m0sm/kg
low plasma osmolality= water excess ( less concentrated) diluted’
high plasma osmolality= water deficit (more concentrated) not diluted/dark urine
hydrostatic pressure
pushes fluid out of vessel
oncotic pressure
pulls fluid into vessel
Fluid shifts
st space: fluid where expected, no edema
nd space: fluid shifts from capillary to interstitial space, edema
rd space: nonfunctional space between cells (ex: ascites)
Antidiuretic Hormone
posterior pituitary hormone
tells kidneys to hold onto fluid
Regulation of Fluid Balance: Hypothalamic Pituitary
osmoreceptors in hypothalamus detect FVD and FVE through increased or decreased plasma osmolality
FVD: hypothalamus stimulates pituitary to secrete ADH
kidneys respond by increasing water reabsorption
increasing osmolality
FVE: hypothalamus tells pituitary to suppress ADH release
kidneys respond by increasing diruesis
decreasing osmolality
Regulation of Fluid Balance: Adrenal Cortex
releases hormones to regulate water and electrolytes
glucocorticoids: cortisol
antiinflammatory effects
inceases blood glucose
mineralocorticoids: aldosterone (when increases it tells kidneys to hold on to urine)
sodium and water reabsorption in kidneys
Renin- Angiotensin- Aldosteron System (RAAS)
activated with hypotension & low perfusion
Goal: conserve water and raise BP
Renin released by. kidneys……
Angiotensin 1 to be converted to Angiotensin 2
Angiotensin 2 is a potent vasoconstrictor which causes secretion of aldosterone
aldosterone from adrenal glands —→ sodium and water reabsorbed into circulation by nephrons'
result: fluid retention to raise BP
Regulation of Fluid Balance: Cardiac
(stretching of atria, opposite of endocrine response)
natriuretic peptides:
atrial natriuretic peptide (ANP)
B type Natriutretic peptide (BNP)
sense increased atrial pressure in fluid volume overload
antagonists to RAAS (suppress aldosterone renin & ADH)
leads to decreased blood volume and BO
Regulation of Fluid Balance: Gastrointestinal
oral intake= most water, including water in foods such as veggies
diarrhea and vomiting can lead to significant fluid and electrolyte loss
Regulation of Fluid Balance: Older Adult Considerations
kidneys: decreased ability to conserve water
endocrine: decrease in renin and aldosterone and increase in ADH and ANP
skin: loss of subq tissue —> to increased moisture lose
Normal Lab Values
BUN
Creatinine
Hematocrit
Urine Specific Gravity
Osmolality
BUN: 7-20 mm/dL
Creatinine: 0.84-1.21 mg/dL
Hematocrit:
M: 41-50%
F: 36-44%
Urine Specific gravity: 1.002-1.030
Osmolality: 280-295 m0sm/kg
Lab values: Fluid defecit
BUN
Creatinine
Hematocrit
Urine Specific Gravity
Osmolality
all lab values increase excepts creatinine remain normal
Lab Values: Fluid Excess
all lab values decrease except creatinine remains normal
Fluid Volume Imbalance
Hypovolemia & Hypervolemia
Hypovolemia
ECF loss > intake
cases: blood loss, GI loses (V/D), insensible loses, sweating, fever
manifestations: dry mouth, skin turgor, decreased urine output
signs/symptoms:4 C’s
Cap refill delayed
confused
cramping
cool and clammy
Hypervolemia
Fluid Retention > Output
causes: fluid in lungs, heart failure, dialysis (renal failure), excessive IV administrration
Manifestations: edema, lung crackles, vein buldge
signs/symp: 3 C’s
crackles
cant catch breath (dyspnea)
cough
Sodium Main Roles
ECF volume and concentration
generation and transmission of nerve impulses
muscle contractility
acid base balance
thirst from thalamus= primary protection against imbalances
sodium imbalances
hyponatremia v hypernatremia
Hyponatrremia
<135 mEq/L
causes: excessive free water intake, diuretic drug (losing), SIADH (increases ADH) syndrome of innappropriate ADH, addisons disease
Manifestations: asymptomatic, N/V/D, mailase, headache, lethargy and disorentiation, seizure and coma
managemet: restrict fluid intake and increase sodium intake
Hypernatremia
>135mEq/L
causes: sweating (decrease fluid), diabetes, hypertonic fluids
manifestations: severe coma and seizures
FRIED
Fever (low), flushed skin
Restless (irritable)
Increased Fluid retention and increased BP
Edema (peripheral and pitting)
Decreased urine output , dry mouth
Management: increase fluid
Potassium Main Roles
transmission and conduction of nerve and muscle impulses
cellular growth
maintenance of cardiac rhythms
acid base balance
think kidneys— excrete 90% potassium: renal damage leads to increase potassium retention
Potassium Imbalance
Hypokalemia v Hyperkalemia
Hypokalemia
causes: GI loss (NG tubve), decreased intake, non potassium sparing diuretic
Manifestation: (A SIC WALT (decrease)- alkalosis, shallow resp, irritability, confused/ drowsiness, weakness/ fatigure, arythmias (irregular rate and tachycardia), lethargy, thready pulse, decreased intestinal motility, N/V, ileus
flattened t waves and prominent U waves
Management: IV potassium and heart monitor
Hyperkalemia
causes: renal dysfunction, addisson’s disease, trauma, excessive administration
Manifestations: muscle twitches— cramps— paresthesia, irritability/anxiety, decreased BP, EKG changes (tented T waves), dysrhythmias= irregular rhythms, abdominal cramping, diarrhea
Management: low potassium diet and heart monitor
Hyperkalemia medications
calcium gluconate
sodium polystyrene
sodium zirconium cyclosilicate
insulin (w/ dextrose)
sodium bicarbonate
Calcium Gluconate
hyperkalemia medication
MOA: stabilizes myocardium
effect: decrease risk of arrythmias
nursing considerations: does NOT decrease potassium
Sodium Polystyrene
hyperkalemia medication
MOA: cation exchange resin
effect: decrease potassium
nursing considerations: dont use with ileus
Sodium Zirconium Cyclosilicate
hyperkalemia medication
MOA: potassium binder
effect: decrease potassium
nursing considerations: dont use w ileus and must jave functioning GI tract
INsulin (w/ dextrose)
hyperkalemia medication
MOA: shift potassium into cell
effect: decrease potassium
nursing consideration: monitor blood glucose
Sodium Bicarbonate
hyperkalemia medication
MOA: shift potassium into the cell
Effect: decrease potassium
nursing consideration: monitor blood glucose
IV potassium Administration
always diluted
infused slowly with infusion pump: 11mEq/hr PIV max and 20 mEq/hr CVL max
monitor urine output: renal impairment —decreased potassium excretion
monitor for signs of phlebitis: potassium can burn veins
avoid digoxin toxicity associated with hypokalemia
Calcium Main Roles
formation of teeth and bone
blood clotting
transmission of nerve impulses
myocardial and muscle contractions
Calcium: Type, Source, Regulation
obtained by ingested foods (need VD to absorb)
present in 3 forms (ionized calcium is biologically active)
changes in pH and serum albumin affect levels
Balance Controlled by hormones:
parathyroid hormone (PH): stimulated by LOW calcium
Calcitonin: stimulated by HIGH calcium
Calcium Imbalance
Hypocalcemia v Hypercalcemia
Hypocalcemia
causes:
hypothyroidism
malabsorption
renal impairment
pancreatis
Manifestations:
Chvosteks
Trousseau’s
Hyperreflexia
seizures
arrythmias
laryngeal spasm / stridor (airway closure)
prolonged QT interval
Management:
PO/IV replacement
Heart monitor
Hypercalcemia
causes:
1/3 cause cancer
hyperparathyroidism
Manifestations:
weakness
fatigue
Hypotension
Arrythmias
Calcium/ kidney stones
shorter QT
constipation
Management:
heart monitor
remove overactive gland
increase hydration
Magnesium Functions
Coenzyme in metabolism of Carbohydrates
Required for DNA and protein synthesis
Blood glucose control
Necessary for ATP production
Muscles
Magneisum Imbalance
Hypomagnesium vs hypermagnesium
Hypomagnesium
causes:
#1 alcohol use disorder
malnutrition
Sign/Symptom:
similar to hypocalcemia (Chvosteks, Trousseau’s, Hyperreflexia, seizures, arrythmias, laryngeal spasm / stridor (airway closure), prolonged QT interval) HYPERTENSION!!
Torsade de pointes ( v fib)
Management: replacement
Hypermagnesium
causes:
#1 renal failure
Sign/Symptoms:
similar to hypercalcemia (weakness, fatigue, Arrythmias’s, Hypotension, Calcium stones, shorter QT)
NO KIDNEY STONES
bradycardia
Management
avoid magnesium foods
Dialysis
Phosphate Function
most is in the bones and teeth in for of calcium phossphate
essential to function of muscle, RBCs, and nervous syste,
involved in acid. base buffering system, ATP production, cellular uptake of glucose, and metabolism of carbs, proteins, fats
Reciprocal relationship with calcium
Phosphate Imbalance
Hypophosphate vs hyperphosphate
hypophosphate
causes:
decreased intake
malabsorption
hyperparathyroidism
malignancy
Signs/Symptoms:
similar to hypercalcemia (weakness, fatigue, Hypotension, Arrythmias, Calcium Stones, shorter QT)
No KIDNEY STONES
Constipation
Acute/mild: may be asymp
Severe: may be fatal, CNS depression, resp/cardiac failure
chronic: osteomalacia
Management:
Phosphate supplementation
osteoporosis
Hyperphosphate
causes:
renal failures
excessive phosphate intake
hypoparathroidism
tumor lysis sysdrom
Signs/Symptoms:
similar to hypercalemia (Chvosteks, Trousseau’s, Hyperreflexia, seizures, arrythmias, laryngeal spasm / stridor (airway closure), prolonged QT interval
neuromuscular irritability
may be asymp
calcium deposists in soft tissues and kidneys
Management:
phosphate binders
avoid phosphate rich foods
diuretics