Ch.8 Fluids and Electrolytes (Final Exam Study Guide)

intracellular, extracellular, interstitial

3 primary fluid types

intracellular

fluid inside cells (an excess will present as edema)

extracellular

fluid not within the cells (in other compartments, such as the blood stream as plasma, lymph, etc.)

interstitial

fluid in the between spaces; when fluid leaches out of the cells into these spaces it is supposed to be just enough to be a cushion

hydrostatic pressure

force of fluid pressure in the bloodstream, pushes water, pumping action of the heart

osmotic pressure

pressure by solutes, pulls water

oncotic pressure

"colloid pressure", pressure due to albumin in blood, keeps water with blood vessels

albumin

is a protein in your blood plasma. keeps fluid from leaking out of your bloodstream. it also helps vitamins, enzymes, hormones, and other substances circulate throughout your body

liver

makes albumin

osmolality

concentration of (active particles) solutes/kg solution

osmolarity

number of osmoses of solute per liter of solution

starling's law of capillary forces

essentially fluid always flows from a higher pressure to a lower pressure

tonicity

amount of solutes in solution compared with the bloodstream

isotonic

same tonicity as blood. does not cause fluid shifts or changes in cell size

normal saline (0.9% NaCl), Lactated Ringer's or Ringer's lactate (similar physiologic constituents as found in blood)

standard isotonic solutions

hypotonic

fewer particles (more water) than blood. pulls water into cells; dehydration. IV infusion shift from ECf to ICF

hypertonic

more particles (less water) than blood. IV infusion pushes water from ICF into ECF

osmoreceptors

located in hypothalamus and stimulated by increased plasma concentration.

thirst mechanism and ADH (antidiuretic hormone)

osmoreceptors initiative ___

ADH (vasopressin)

stimulates kidney nephron to reabsorb more water

renin-angiotensin-aldosterone system (RAAS)

a hormone cascade pathway that helps regulate blood pressure and blood volume

hypotension, hypovolemia, low cardiac output

the renin-angiotensin-aldosterone system (RAAS) activates due to ___

renin released from kidneys- kidneys kick in when they are not getting enough blood

-converts angiotensinogen (from liver) to angiotensin I (in the lungs)

step 1 in renin-angiotensin-aldosterone system (RAAS)

angiotensin I converts to angiotensin II

-in the lungs by angiotensin converting enzyme (ACE)

step 2 in renin-angiotensin-aldosterone system (RAAS)

angiotensin II (vasoconstrictor)

-activated adrenal cortex to release aldosterone

step 3 in renin-angiotensin-aldosterone system (RAAS)

aldosterone

-increases sodium and water reabsorption and potassium excretion by kidneys

step 4 in renin-angiotensin-aldosterone system (RAAS)

natiuresis

is the opposite of RAAS-when too much volume- body kicks into ___ to release fluid

atrial natriuretic peptide (ANP), b-type natriuretic peptide (BNP), c-type

3 peptides that promote/initiate natriuresis

atrial natriuretic peptide (ANP)

atrial cells when atria is stretched-released from atria. too much fluid causes the muscle to stretch, when the stretch occurs, this peptide is released

B-type natriuretic peptide (BNP)

-in the heart ventricles

-most clinical applications; measured using lab values primarily coming from the heart (heart failure)

-direct measure of stretch happening in ventricles-this stretch causes the release of ___

-when body systems fail, this ___ will keep releasing to try to get back to normal-indicates exacerbated heart failure

swelling/edema

fluid accumulation in ICF and ISF

elevated hydrostatic pressure

-increased ECF volume as occurs in heart failure

decreased osmotic forces in blood

-hypoalbuminemia (liver failure, protein malnutrition)

alterations in capillary permeability

-histamine

-inflammation

sodium retention

-due to illness or consumption of salty foods

-pulls fluid from ICF into ECF

primary causes of edema

transudate

serous filtrate of blood

exudate

contains lymph, blood, proteins, pathogens, inflammatory cells (due to infection, trauma, injury- basically it's all the stuff that travels to the site to help)

hypervolemia (fluid volume overload)

bloodstream has excessive amount of water

heart failure

one of the most common causes of hypervolemia is ___

edema

in hypervolemia, ___ develops due to high hydrostatic forces (force of fluid pressure in bloodstream-pushes water)

-changes in LOC

-confusion

-headache

-seizures

-pulmonary congestion

-bounding pulse

-increased BP, increased jugular vein distention

-tachycardia

-anorexia

-nausea

-edema

hypervolemia will manifest ___

Hypovolemia (fluid volume deficit-dehydration)

when extracellular volume is low, it starts to pull fluid from tissues, drying them out because of osmosis, so ECF is now the area of low concentration. natural fluid flows there to achieve homeostasis-activates thirst signals in hypothalamus, released ADH, turns of circulatory system, increasing heart rate by vasoconstriction

tachycardia and hypotension

decreased circulating blood volume leads to ___

-reduced fluid intake

-reduced ADH or kidneys not responsive to ADH

-excessive sweating

-burns, fever, perspiration

-osmotic diuresis-associated with high glucose levels

-hypernatremia -water follow sodium

causes of hypovolemia

-changes in skin turgor

-tachycardia

-weak pulse

-postural hypotension

-confusion

-thirst

-dry skin

-sticky, dry mucous membranes

-weight loss

-concentrated urine

-tiredness

-headache

-constipation

-dizziness

-low BP

hypovolemia will manifest as ___

sodium

is a major ion in ECF- ___ will always have a higher concentration in ECF (outside of the cell)

potassium

is a major ion in ICF- ___ will always have a higher concentration in ICF (inside of the cell)

sodium/potassium pump

-fuel for nerve conduction

-keeps K+ inside the cell and moves Na+ into vasculature

-imbalances in either sodium or potassium disrupt normal functions

we start with 3 Na_ irons and 1 ATP

step 1 in sodium/potassium pump

ATP splits providing energy to change the shape of the channel. sodium ions are driven through the channel

step 2 in sodium/potassium pump

the Na+ ions are released to the outside of the membrane, and the new shape of the channel allows two K+ ions to bind

step 3 in sodium/potassium pump

release of the phosphate allows the channel to revert to its original form, releasing the K+ ions on the inside of the membrane

step 4 in sodium/potassium pump

135-145 mEq/L

normal sodium levels

hyponatremia

low sodium in the blood, less than 135 mEq/L

adrenal insufficiency, osmotic diuresis, diuretic use

renal causes of hypovolemic hyponatremia

primarily GI losses: excessive sweating, diarrhea, vomiting

non-renal causes of hypovolemic hyponatremia

Nausea, vomiting

GI suctioning

headache

behavior changes

decreased LOC

confusion

lethargy

seizures

thirst

dry mucous membranes

low urine output

hypotension

tachycardia

clinical manifestations of hypovolemic hyponatremia

slowly replace sodium, hypertonic solutions

hyponatremia treatment

syndrome of inappropriate antidiuretic hormone (SIADH)

example of hypervolemic hyponatremia

hypernatremia

more than 145 mEq/L

breastfed infants, fever, vomiting, diarrhea, excess sweating, risk in elderly due to decreased thirst mechanism

causes of hypovolemic hypernatremia

dehydrated

thirst

tachycardia

hypotension

decreased urine output

clinical manifestations of hypovolemic hypernatremia

re-hydrate

hypovolemic hypernatremia treatment

diabetes insipidus

causes of hypervolemic hypernatremia

edema

weight gain

hypertension

pulmonary edema

dyspnea

clinical manifestations of hypervolemic hypernatremia

fix underlying cause. prevent dehydration with hypotonic solutions, sodium restricting diet, giving diuretics

hypervolemic hypernatremia treatment

disorientation

hallucinations

agitation

restlessness

confusion

seizures

lethargy

agitation

orthostatic hypotension

dry, flushed skin

overall signs and symptoms of hypernatremia

Cushing;s syndrome- think round, swollen, moon face

hypernatremia is associated with ___

3.5-5.2 mEq/L

normal potassium levels

hypokalemia

serum K+ less than 3.5 mEq/L

burns, vomiting, diarrhea, GI suctioning, diuretics, laxatives, insulin

causes of hypokalemia

anorexia

nausea

vomiting

constipation

orthostatic hypotension

cardiac arrhythmias

leg cramps

muscle weakness, from lower to upper extremities

U waves on EKG, low T waves

wide QRS complex

hyporflexia-decreased, weak responses

clinical manifestations of hypokalemia

replace K+ through foods, oral medicine

hypokalemia treatment

IV push

___ will kill patient with hypokalemia

hyperkalemia

serum K+ greater than 5.2 mEq/L. rapid onset is worse than chronic

kidney disease/failure, burns, Addison's disease, ACE inhibitors, K+ sparing diuretics, excessive intake of salt substitutes

causes of hyperkalemia

early symptoms-numbness, muscle spasms

paresthesia-"pins and needles"

diarrhea

bradycardia

ECG-tall peaked T waves

clinical manifestations of hyperkalemia

8.7-10 mg/dL

normal range for calcium

calcium

involved with bones, teeth, blood clotting, neuromuscular signaling

hypocalcemia

serum level less than 8.7 mg/dl

insufficient dietary intake of calcium and/or vitamin D, vitamin D deficiency, malabsorption, hypoparathyroidism

causes of hypocalcemia

parathyroid gland

controls calcium

alcohol abuse

risk of hypocalcemia

chvostek's sign-face twitching

trousseau's sign-spasm of hand and arm

increased deep tendon reflexes

QT prolongation (decreased MI)

tetany-intermittent muscular spasms

decreased bone density

clinical manifestations of hypocalcemia

paresthesia

-hands, mouth, feet

muscles spasms

severe

-hypotension

-cardiac arrhythmias

-laryngeal spasm (wheezing, bronchospasm, dysphagia, stridor)

seizures

acute clinical manifestations of hypocalcemia

bone pain and fragility

dry skin/hair

cataracts

depression

dementia

neuromuscular excitability/tetany

-chvostek's sign

-trousseau's sign

chronic clinical manifestations of hypocalcemia

seizure precautions

for hypocalcemia patient would be on ___

oral and IV replacement of calcium

hypocalcemia treatment

hypercalcemia

serum Ca+ greater than 10 mg/dL

elevated parathyroid hormone, cancer, excess calcium/vit D intake, prolonged immobility, chelating drugs loop diuretics

causes of hypercalcemia

decreased neuromuscular excitability

decreased deep tendon reflexes

decreased GI motility

constipation

nausea/vomiting

anorexia

ulcers

hypertension, bradycardia

renal calculi

cardiac arrhythmias

lethargy

QT shortening

clinical manifestations of hypercalcemia

encourage client to increase water intake

hypercalcemia treatment

renal calculi

patients with hypercalcemia have an increased risk for ___

calcium and phosphorous

are enemies; one goes one way and the other goes the other way

2.5-4.5 mg/dl

normal phosphorus levels

phosphorous

component of bone, RBCs, ATP, enzymatic processes, acid-base balance

combines with oxygen to form phosphate

hypophosphatemia

serum levels less that 2.5 mg/dL

decreased intestinal absorption, increased excretion by kidneys, intracellular shift, referring syndrome, Cushing syndrome, malabsorption/starvation, chronic use of aluminum-based antacids, hyperparathyroidism

causes of hypophosphatemia

confusion

apprehension

muscle weakness

diaphragmatic dysfunction

-respiratory insufficiency

RBC, WBC, platelet dysfunction

bone pain

joint stiffness

clinical manifestations of hypophosphatemia

hyperphosphatemia

serum levels greater than 4.5 mg/dL

most common cause is kidney failure

then hypoparathyroidism, rhabdomyolysis, tumor lysis, metabolic/respiratory acidosis

causes of hyperphosphatemia

hyperreflexia

soft tissue calcification

tetany

bone and joint pain

parasthesias

delirium

convulsions

seizures

hypotension

ECG: prolonged QT interval

clinical manifestations of hyperphosphatemia

1.5-2.5 mEq/L

magnesium normal range