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Less volume
Less pressure
More volume
More pressure
Transcellular
Can’t access
Urine, swear, digestive secretions, CSF
Electrolytes
Substance whose molecules dissociate into ions when placed in water
What are some examples of cations?
Na
K
Mg
Ca
What are some examples of anions?
Cl
PO43
HCO3
What do electrolytes help do?
Regulate and maintain pH in the body
Essential for activity of body system
To function normally, body cells must have fluid and electrolytes in?
The right COMPARTMENT and right AMOUNT
What separates the compartments?
Semipermeable membranes
Body fluids
Transport nutrients to the cell and then carry waste products from the cells
Water accounts for % of an adult's total weight?
60
Diffusion
A solute moves through a solvent across a permeable membrane from high to low concentration requiring NO energy source
Facilitated diffusion
Bigger particles/solute (like glucose) moves through a solvent across a permeable membrane from high to low concentration requiring NO energy source, BUT does require help from a protein carrier
Osmosis
Movement of only water across a membrane from a low to higher concentration requiring NO energy source
Active transport
Movement of everything across a membrane from a low to higher concentration requiring ATP since it is going against the gradient
Osmotic pressure
Force created by solutes that pulls water toward them across a semipermeable membrane
More solutes there are, greater the pull
“Salt Sucks”
The higher concentration of solutes
The greater the osmotic pressure or pulling power
Trick for OsmoLALITY
Sounds like reALITY
Prefer to live in reality
Osmolality
Number of solute particles per kilogram
mOsm/kg
More precise / preferred
Osmolarity
Solutes per liter of solution
mOsm/L
Hypotonic solution
Solutes are less concentrated than in cells
Hypoosmolar
Water moves into cell, causes swelling / potential bursting
Hippo
Isotonic solution
Same as cell interior
No major fluid shift
Hypertonic solution
Solutes are more concentrated than in cells
Hyperosmolar
Water moves out of cell, causes shrinkage / potential cell death
Hypotonic %
0.45%
Isotonic % (baseline, what we want)
0.9%
Hypertonic %
3%, 5%
What are all the systems that help fluids get regulated?
Renal
GI
Hypothalamic-Pituitary
Adrenal Cortical
Cardiac
Renal Regulation
Kidneys filter & secrete
Intake & Output
Intake: Oral & IV
Output: excretion & insensible losses
GI Tract regulation: Diarrhea & Vomiting
What can we use as an indicator of overall fluid volume loss or gain?
Daily weights
Strict I&O’s
Renal tubules are sites of action of
ADH and aldosterone
Hypothalamus =
Sensor + Thirst Center
Hypothalamic- Pituitary regulation
Hypothalamus detects deficit of fluids
Signals the Posterior Pituitary to release ADH
ADH then increases water reabsorption
Adrenal cortical regulation
Activates RAAS (Renin-Angiotensin-Aldosterone System) which triggers the release of Aldosterone to “hold on” to sodium and water while excreting potassium.
When would the adrenal cortical regulation trigger RAAS to release Aldosterone?
Low BP / Low Blood Volume [think dehydration]
Low Sodium levels
High Potassium levels
Cardiac regulation
ANP [Atrial natriuretic peptide] & BNP [B-type natriuretic peptide]
Made by myocardial cells
Released in response to increased pressure within heart chambers to stimulate the ELIMINIATION of water & sodium in urine
INHIBITS ADH & RAAS
Patient excretes more urine
ANP is released from the
Atria
BNP is released from the
Ventricles
Hypovolemia
Decreased circulating blood volume
Loss of water & electrolytes in equal proportions
Dehydration
Loss of water alone
Hypervolemia
Increased circulating blood volume
Too much water & electrolytes
Overhydration
Too much water alone
Hypovolemia S/S
VS: ↑ HR, ↓BP, ↓CVP, ↑ RR, ↓ O2 sat, ↑ or ↓ temperature
CV: Thready pulse, ↓ cap refill, flattened neck veins
Neuro: Dizziness, syncope, confusion, weakness, fatigue, seizures
GI: Thirst, dry mucosa, nausea, vomiting, anorexia, acute weight loss
GU: Oliguria
Skin: Cool & clammy, diaphoresis, poor skin turgor & tenting
Other: sunken eyeballs
Hypervolemia S/S
VS: ↑HR, ↑ BP, ↑ CVP, ↑ RR
CV: Bounding pulse, distended neck veins
Respiratory: Crackles, cough, dyspnea
Neuro: Weakness, visual changes, paresthesia, altered LOC, seizures (if sudden hyponatremia water excess)
GI: Ascites, ↑motility, liver enlargement, weight gain
GU: ↑ urine output, dilute urine
Skin: Peripheral edema, cool with pallor
When would we use IV therapy?
Unable to take substances orally
Replace water, electrolytes, and nutrients more rapidly
Provides immediate access to vascular system
Crystalloids
Aqueous solution of mineral salts and other small, water-soluble molecules
Contain no proteins or colloids
Low cost
Short half-life
Fewer side effects
Hypotonic, isotonic, hypertonic
Colloids
Stay in vascular space & increase oncotic pressure
Large insoluble molecules
Do not diffuse through membranes easily
All colloids affect blood coagulation, by interfering with coagulation factor VII
Human plasma products (albumin, fresh frozen plasma, blood)
Semisynthetics (dextran and starches, [hespan])
Isotonic solutions
Ideal to replace ECF volume deficit due to acute loss, such as diarrhea, blood loss
Same osmolality as body fluids
0.9% Sodium Chloride [Normal Saline, NS, Saline]
Lactated Ringer’s Solution
0.9% Sodium Chloride [Normal Saline, NS, Saline]
Used when both fluid and sodium are lost
Only solution used with blood
Lactated Ringer’s Solution
Contains sodium, potassium, chloride, calcium & lactate
Expands ECF – ideal for surgery, trauma, burns & GI losses
Remember, if your ECF volume is too low, your body faces risks like low BP, organ injury, etc.
Caution with liver disease since it contains lactate
If your liver can’t metabolize lactate and convert to bicarbonate = metabolic issues (lactic acidosis)
Hypotonic solutions
0.45%NS, D5W
0.45%NS, D5W
More dilute solutions & have a lower osmolality than body fluids
Cause movement of water into cells by osmosis – Dilutes ECF because more solvent than solute
Replace deficits of total body water
Hydrate cells but can deplete circulatory system
Usual choice for maintenance fluids but should be administered slowly to prevent cellular edema
Monitor for changes in mentation because of cellular edema
When would you not give hypotonic solutions?
Patient’s at risk for increased ICP
Extensive burn or trauma – they are already hypovolemic – will worsen
Hypotonic D5W- 5% Dextrose
Behaves differently in the bag vs. in the body!
5 grams of dextrose per 100mL
Technically isotonic in the bag, but hypotonic in the body
Since the dextrose is rapidly metabolized!
Hypertonic solutions
D5W in NS (D5NS) or D5W in 0.45% NS (D5 ½ NS)
D5 ½ NS more common
D5W in LR (D5LR)
D10W or D20W or D50W
3% or 5% NS (most common)
D5W in NS (D5NS) or D5W in 0.45% NS (D5 ½ NS)
D5W in LR (D5LR)
D10W or D20W or D50W
3% or 5% NS
Higher osmolality compared with plasma
Draws water out of cells into ECF
Electrolyte replacement & shift fluid from cells to vascular space
Requires frequent monitoring of BP, lung sounds, serum sodium levels
Since it can cause fluid overload
Colloid solutions
Dextran
Hetastarch (Hespan)
Dextran
Volume expander
Monitor for circulatory overload / increased bleeding
No electrolytes included
Increases plasma volume by 1 to 2 times
Increases urine output
Treatment for severe hypovolemic shock, burn-related shock, hemorrhage, surgery, trauma
First 500ml – give at 20-40 ml/hr if hypovolemic; reduce rate if additional volume is required
Slow administration
Trick to remember dextran
Dextran = Detour
it is not a permanent solution and is only temporary
Hetastarch (hespan)
Synthetic colloid volume expander
Lasts 24-36 hours
Treatment & prevention of dangerously low BP / hypovolemia
For both dextran and hetastarch (hespan) always monitor for
Fatal anaphylactic reactions
Albumin
“Protein puller”
Pulls proteins back into blood to expand volume
Equivalent to plasma
Available is 5% and 25% solutions
Used to treat hypoproteinemia in burns and hypoalbuminemia in shock and ARDs
Used to support blood pressure in dialysis and acute liver failure
Mannitol
Osmotic Diuretic
Makes water move to extracellular & vascular spaces
Comes in 5%, 15%, 20%, 25% solutions
No dilution required
All crystals must be dissolved to infuse
Treatment of ARF, cerebral edema (decreases ICP), generalized edema
Monitor electrolytes – may induce dehydration with hyperkalemia, hypokalemia, or hyponatremia
20% & 25% solutions are vesicants
NCLEX – Requires caution with impaired cardiac or renal systems (contraindicated with anuria, severe pulmonary & cardiac congestion, & intracranial bleeding)
Vesicants
Medications or solutions that can cause tissue damage (necrosis or blistering) if they leak out of the vein during intravenous (IV) administration.
Trick for mannitol
Mannitol = “Magnet” for water
Brain, eyes, kidneys
Na+
135-145 mEq/dL
Major ECF cation
Movement: Diffusion through active transport that is controlled by the sodium-potassium pump
Forms: Sodium chloride & sodium bicarbonate
Regulation: Controlled by kidneys through the action of aldosterone
Functions:
Maintains fluid balance
Generating and transmitting nerve impulses, muscle contraction
Acid-base balance
Blood pressure
Imbalances are typically associated with parallel changes in osmolality
Causes of hypernatremia
Water loss
Hyperventilation
Heat stroke
Insufficient ADH - Diabetes insipidus
Loss of thirst mechanism
Inadequate water intake
Causes of hyponatremia
Drinking water for fluid replacement
Inadequate sodium intake Loss of sodium-containing fluids
Psychogenic polydipsia
D5W
Hormonal imbalances - insufficient aldosterone, adrenal insufficiency, SIADH
S/S of hypernatremia
Fluid shift out of the cells due to increased osmotic pressure of interstitial or extracellular fluid
Thirst; tongue and mucosa dry and sticky
Weakness, lethargy, agitation
Edema
Elevated BP, tachycardic
Decreased urine output
S/S of hyponatremia
Impairs nerve conduction
Muscle cramps, abdominal discomfort or cramps with nausea & vomiting, anorexia
Fatigue, lethargy, muscle weakness;
Late - shallow, ineffective respiratory movement R/T skeletal muscle
Decreased osmotic pressure in extracellular compartment causing fluid shift into cells resulting in hypovolemia & decreased BP
Swelling in brain - confusion, headache, weakness, seizures; late – coma
Tx for hypernatremia
Restrict sodium
Dilute with sodium-free fluids to make sodium go down
Daily weights
I & O
Recheck labs
Tx for hyponatremia
Fluid restriction
Needs sodium
Hypertonic saline if having neuro problems
3% or 5% NS
Severe hyponatremia
Sodium [Na] <120 mEq/L
Severe symptoms such as seizures, coma
Give small amount of IV hypertonic saline solution (3% NaCl)
Regardless of the cause or severity…
At risk for osmotic demyelination injury if hyponatremia is corrected too quickly
Monitor for lithium toxicity because hyponatremia slows lithium excretion
Monitor frequent VS, strict I & O, serial sodium levels
K +
3.5-5.0 mEq/dL
Major ICF cation
Regulated by the kidneys
Necessary for
Resting membrane potential of nerve and muscle cells
Regulates intracellular osmolality
Promotes cellular growth
Maintenance of cardiac rhythms
Acid-base balance
Tricks to remember for potassium
King inside= Major ICF cation
“About 3-5 bananas in each bunch… want them half ripe so 3.5-5”
Potassium pumps
Causes for hyperkalemia
Renal failure
Deficit of aldosterone
Potassium-sparing diuretics – spironolactone
Massive cell destruction
Metabolic acidosis
Catabolic states (severe infections)
Causes for hypokalemia
Abnormal losses from kidneys or GI tract
Excessive aldosterone or glucocorticoids (Cushing’s syndrome)
Decreased dietary intake - alcoholism, eating disorders, starvation
Treatment of diabetic ketoacidosis with insulin
S/S for hyperkalemia
Cardiac dysrhythmias & conduction
Bradycardia
Prolonged PR interval, flat or absent P waves
Widened QRS complex
Depressed ST segment
Tall & peaked T waves
Conduction blocks, ventricular fibrillation
S/S for hypokalemia
Cardiac dysrhythmias - prolonged repolarization and eventual arrest
Slightly prolonged PR interval, peaked P wave
ST depression
Shallow T wave
Prominent U waves
Lethal ventricular - PVCs, ventricular tachycardia
Tx for hyperkalemia
Sodium polystyrene sulfonate
Dialysis
Tx for hypokalemia
PO or IV potassium chloride “K-riders”
Causes GI upset - give with food
Assess output before & during administration
Increase dietary potassium
Trick to remember K-containing food
The thanksgiving song “Greens, beens, potatoes, tomatoes…”
Steps to treat hyperkalemia
Stabilize
Stabilize cardiac cell membrane by administering calcium chloride or calcium gluconate IV
Does not drop K levels but stabilizes heart
Force
Force K+ from ECF to ICF by IV regular insulin with dextrose and a ß-adrenergic agonist or sodium bicarbonate
Monitor
Use continuous ECG monitoring
Potassium administration (everything very very important)
NEVER give IV Push, IM injection, or SQ injection!
Always dilute IV KCl (10mEq in 100 mL)
Never give by gravity – need an infusion pump
Should not exceed 10 mEq/hr unless in critical care with cardiac monitoring
Irritant
Monitor IV site frequently & stop immediately for signs of phlebitis or infiltration
Ca2+
9.0-10.5 mg/dL
ECF cation
Formation of teeth and bone
Blood clotting
Transmission of nerve impulses
Muscle contraction
Myocardial contractions
Ingested in food, stored in bone, and excreted from the body in the urine and feces
Controlled by parathyroid hormone (PTH) and calcitonin, but it is also influenced by vitamin D and phosphate ion levels.
Calcium and phosphate ions in the extracellular fluid have a reciprocal relationship.
Causes of hypercalcemia
Uncontrolled release of calcium ions from the bones
Hyperparathyroidism causes ⅔ of the cases
Cancer - hematologic, breast, or lung
Thiazide diuretics
Immobilization
Increased intake of calcium due either to excessive vitamin D or excess dietary calcium
Causes of hypocalcemia
Decrease in the production of parathyroid hormone
Radical neck surgery
Malabsorption syndrome
Deficient serum albumin
Alkalosis
Renal failure
S/S of hypercalcemia
Depress neuromuscular activity, leading to
Muscle weakness, loss of muscle tone, lethargy, and stupor
Apathy, personality changes, anorexia, and nausea
Anorexia, nausea, constipation
Interferes with the function of ADH in the kidneys
Less absorption of water
Polyuria, thirst
Cardiac
Contractions increase in strength
Dysrhythmias may develop
Increased BP
Effects on bone vary with the cause of hypercalcemia.
If excess PTH is the cause, bone density will be decreased
If intake of calcium is high, PTH levels will be low, and more calcium will be stored in the bone, maintaining bone strength.
May contribute
Shortened version to remember hypercalcemia s/s
Stones
Kidney stones
Bones
Bone pain, fractures
Groans
Abd. pain, constipation, N/V
Thrones
Polyuria, dehydration, sitting on throne (toilet)
Psychiatric moans
Confusion, lethargy, depression
S/S of hypocalcemia
Increase in the permeability and excitability of nerve membranes
Spontaneous stimulation of skeletal muscle > muscle twitching, carpopedal spasm, and hyperactive reflexes
Laryngospasm
Paresthesia
Abdominal cramps
Mental confusion, irritability
Heart contractions become weak, delayed conduction, arrhythmias develop, & BP drops
Tests for hypocalcemia
Chvostek’s sign
Trousseau’s sign
Chvostek’s sign
“Cheek”
Contraction of facial muscles in response to a light tap over the facial nerve in front of the ear
Trousseau’s sign
“Tourniquet (BP cuff)”
Carpal spasm induced by inflating a BP cuff above the systolic pressure for a few minutes
Tx for hypercalcemia
Restricting dietary calcium
Promoting urinary calcium excretion with loop diuretics
Hydrating the patient with isotonic saline infusions
Move!
Safety precautions
Medications that decrease serum Ca:
Bisphosphonates
Calcitonin
Tx for hypocalcemia
Oral or IV calcium supplementation
Vitamin D
Phosphate binders to excrete phosphate & ↑ Ca
Sevelamer hydrochloride
Calcium acetate
Calcium imbalance meds.
IV 10% calcium gluconate
Administer medications that increase calcium absorption
Aluminum hydroxide reduces phosphorus levels, causing the countereffect of increasing calcium levels
Vitamin D aids in the absorption of calcium from the intestinal tract
IV 10% calcium gluconate
Warm injection solution to body temperature, administer slowly, monitor for ECG changes, observe for infiltration
Stabilizes heart
Hypocalcemia safety
Provide a quiet environment to reduce environmental stimuli
Initiate seizure precautions
Move the client carefully, and monitor for signs of pathologic fracture
Calcium-containing food
Dairy products
Tofu
Green leafy vegetables
Salmon & sardines
Almonds
Sunflower seeds
Dried beans
Molasses
PO43-
3.0-4.5 mg/dL
Primary anion in ICF
Essential to function of cell membrane regulation, muscle, RBC, nervous system
Involved in acid-base buffering system, ATP production, cellular uptake of glucose, and metabolism of carbohydrates, proteins, and fats
Found mostly in bones & teeth
Reciprocal relationship with calcium
Imbalances are typically, asymptomatic – problems are associated with hypo & hypercalcemia
Causes of hyperphosphatemia
Acute kidney injury or chronic kidney disease
Tissue damage or cancer chemotherapy