F&E Flashcards
Extra cellular fluid
1/3 body fluid
14L
Made up of interstitial fluid and vascular fluid
Main electrolytes sodium and chloride
Intracellular fluid
2/3 body fluid
28L
Most stable
Main electrolytes are potassium and phosphate
Osmosis
Water moved from low concentration to high concentration through semi- permeable membrane
Cell membranes or capillary membranes are the permeable membrane
Passive movement
Diffusion
Solutes move from high to low concentration
Passive movement
Active transport
Cell membranes move molecules
Low concentration to high concentration
Requires metabolic work (ATP)
Ex. K, Na, H, Fe, Cl, I
Osmolality
Concentration of solute per Kg of h2o
Higher the osmolality the greater it’s pulling power for water
Osmolality
Concentration of solute per L of solution
1L water=1Kg
Serum osmolality
Concentration of particles in the plasma
Normal=275-295milliosmoles/L (mOsm/L)
Sodium is major solute in plasma
Number 1 lab for checking fluid deficit/status
Urea (BUN) and glucose increase serum osmolality
Capillary filtration
Hydrostatic pressure and oncotic pressure
Hydrostatic pressure
Pushing force of fluid against the walls of the space it occupies. ( pushing out)
Oncotic pressure (colloid osmotic pressure)
Pulling force of proteins in vascular space. (Pulling in)
Chemical regulation of fluid balance
Antidiuretic hormone (ADH) Aldosterone Glucocorticoid (cortisol) Atrial natriuretic peptide (ANP) Brain natriuretic peptide (BNP) Thirst sensation
Nephrons filter how many liter per day?
150-180L/day
This is glomerular filtration rate (GFR)
If body looses 1-2% body fluid then conservation begins
ADH (vasopressin)
Hypothalamus->post pituitary-> distal tubules regulate water
Decrease Blood pressure or volume or rise in blood osmolality = excretes ADH to conserve water
Rise in BP or blood volume then drop in blood osmolality = inhibits ADH ( excretes water)
Aldosterone
Adrenal gland -> kidneys retain Na & water & excrete K
Decrease bp, blood volume and Na increase K= reabsorb Na & water follows Na= blood volume increases
Rise in bp or volume or Na & drop in K= excrete Na & water follows Na= blood volume decreases
Glucocorticoids
Cortisol released by adrenal gland
Stress
Causes kidneys to retain Na & water
ANP (atrial natriuretic peptide)
Released when atria stretched Lowers bp and blood volume Causes vasodilation Decreases aldosterone Decreases ADH Increases glomerular filtration rate= more urine production and water excretion
BNP ( b-type natriuretic peptide)
Released when ventricles stretched Lowers blood volume & bp Causes vasodilation Decreases aldosterone Dieresis of water and Na
Thirst
Small shift in serum osmolality
Receptors in hypothalamus detect 1 mOsm/L changes
Stimulate ADH and aldosterone
30-60 min for fluid to be absorbed & distributed
Daily sensible fluid output
Kidneys-1500ml/day
Intestines- 100ml/day
Daily insensible fluid output
Skin-600ml/day
Lungs-400ml/day
Total daily fluid output
2600ml
Daily fluid intake
Liquids- 1500ml
Solid food- 800ml
Water of oxidation-300ml
Total= 2600ml
Isotonic FVD
Fluid and solute lost in proportional amounts
Most common
Hypotonic FVD
Greater loss of electrolytes than water
Decreased plasma osmolality
Hypertonic FVD
More water is lost than solute
Increased plasma osmolality
Acute weight loss or gain
Mild FVD:2%
Moderate FVD: 5%
Severe FVD: 8% or more
Isotonic fluid loss (causes)
Not enough intake Excessive GI fluid loss Excessive renal loss Excessive skin loss Third space lost
Hypertonic dehydration (causes)
Inadequate fluid intake Prolonged or severe isotonic fluid losses Watery diarrhea Diabetes insipidus ( no ADH secreted) Increase solute intake
Isotonic IV fluids
Same osmolality as normal plasma Replaces ECF and electrolyte losses Used to expand volume quickly No calories or free water 0.9% NaCl Ringers solution Lactated ringers solution (LR) 5% dextrose in water (becomes hypotonic)
Hypotonic IV fluids
Lower osmolality than normal plasma Used to prevent/treat cellular dehydration Contraindicated in acute brain injuries Requires freq VS, LOC, circulation 1/2 NS (.45% NaCl solution) 1/4 NS ( .225% NaCl solution)
Hypertonic IV fluids
Higher osmolality than normal plasma Limited doses Use infusion pump Frequent close monitoring 3% sodium chloride 5% sodium chloride D10W (10% dextrose in water) 50% dextrose D51/2NS, D5NS, D5LR, D51/4NS
Isotonic FVE
(Hypervolemia & edema)
Proportional gain in fluid& solute
Excess interstitial fluid volume
Isotonic FVE causes
Renal failure Heart failure Excess intake High corticosteroid levels High aldosterone levels
Hypotonic FVE
( water intoxication)
More fluid than solute gained
Serum osmolality falls
Hypotonic FVE causes
Plain water irrigation Hypotonic IV fluids Over zealous plain water intake Infants-diluted formula SIADH ( syndrome of inappropriate ADH) Psychogenic polydipsia Severe or prolonged FVE w/ existing disease states
Edema causes
Increased capillary hydrostatic pressure -caused by hypertension & hypervolemia Decreased capillary oncotic pressure -decreased albumin - injury, inflammation, malnutrition, liver dysfunction Lymphatic obstruction or removal Sodium excess
Assessment of FVE
Bulging fontanels High CVP w/ venous engorgement Third spacing - peripheral edema - pulmonary edema - ascites Vital signs
Interventions for FVE
Restrict fluid intake Promote excretion - diuretics - digoxin, ACE inhibitors - protein intake Monitor during therapy Prevent more FVE Remain alert for acute pulmonary edema Patient education
Eval of corrected FVE
Resolves edema, soft flat fontanels Lungs- clear, unlabored VS- return to baseline LOC-return to baseline Labs- return to baseline Weight- return to baseline Resolution of underlying causes Verbalize understanding
Sodium range
135-145 mEq/L
Sodium balance & imbalance
Normal ECF range 135-145mEq/L
Responsible for water balance & determination of plasma osmolality
Attracts chloride
Assists w/ acid-base balance
Promotes neuromuscular response & stimulates nerve & muscle fiber impulse transmission
Hyponatremia
<135 mEq/L
Occurs in hypervolemia,euvolemia, & hypovolemia
Hyponatremia cellular transport/ response
- Low Na in ECF-> fluid shift to ICF due to response of decreased plasma volume (baroreceptors), ADH, aldosterone
- edema results
- cerebral edema- demyelination
Hyponatremia causes
Actual
Inadequate Na intake
Loss of body fluid
NPO
Relative (dilution)
Hyperglycemia
SIADH
Irrigation w/ hypotonic fluids
Hyponatremia assessment
- signs related to nerve impulse transmission & muscle contraction
- cardiovascular
- integument
- renal
- neuromuscular
- gastrointestinal
Nursing dx for Hyponatremia
Risk for excess fluid volume Disturbed sensory/perception Risk for injury Impaired oral mucous membranes Disturbed thought processes Risk for impaired skin integrity
Interventions to correct Hyponatremia
Replacement therapies Oral- Parenteral- Continued monitoring Restoration of balance
Hyponatremia + hypvolemic
Correct ECF deficit
Hyponatremia + hypervolemia
Treat underlying cause
Acute Hyponatremia
Hypertonic solution
Hypernatremia
> 145 mEq/L Euvolemic, hypervolemic, hypovolemic Cells shrink Increased neurological activity occurs Thirst mechanism responds
Hypernatremia causes
Actual Excessive ingestion Hyperaldosteronism Corticosteroid Renal failure
Relative NPO Increase metabolism Watery diarrhea Hyperventilation
Assessment of Hyponatremia
- related to cellular dehydration and Na role in nerve impulses & muscle contraction
- tachycardia, NPH, decreased cardiac contractility
- skin dry, sticky, flushed, rough dry tongue
- CNS irritability
- watery diarrhea, nausea, thirst
- if slow rise, may be asymptomatic for some time
Lab findings for Hypernatremia
Na elevated Increased u.o, SG 1.015-1.030 Elevated Cl Serum osmolality >290 mOsm/kg Incresed BUN and Hct
Risk factors for Hypernatremia
Age
Medications
Diet
Nursing dx for Hypernatremia
Risk for injury
Risk for DFV
Disturbed sensory/perception
Impaired oral mucous membranes
Interventions for Hypernatremia
Decrease Na intake
Promote Na excretion
Continued monitoring of client
Restoration of balance
Hypernatremia + euvolemic
Water, identify the cause
Hypernatremia + hypovolemia
NS then D5W
Hypernatremia + hypervolemia
Remove source of excess, diuretics, water
Normal potassium range
3.5-5.0 mEq/L
Potassium balance & imbalance
Normal serum range3.5-5.0 mEq/L
K shifts w/ H
Insulin & catecholamines (epinephrine) increase cellular uptake of K
Adequate intake 40-60 mEq/Day
Adequate K intake
40-60 mEq/day
Hypokalemia
<3.5 mEq/L
Actual Hypokalemia= loss of K or inadequate intake
Inadequate intake
Excessive renal losses- loop diuretics
Excess GI losses
Relative Hypokalemia= K moves ECF to ICF transcompartmental shift
Alkalosis causes K to migrate into cell as H moves out
Increases insulin= K goes to skeletal muscle & hepatic cells
Tissue repair
Water intoxication
Clinical manifestation of Hypokalemia
Rarely develops before drop below 3.0 mEq/L unless drop is rapid
- cardiovascular- increase risk of digoxin toxicity
- respiratory-metabolic alkalosis
- renal- unable to concentrate urine
- GI
- neuromuscular
- CNS
Monitoring Hypokalemia
Serum potassium
ECG changes
Electrolyte levels
I & O
Lab findings for Hypokalemia
Plasma levels- trending
Elevated pH & bicarb levels ( alkalosis)
Elevated glucose
- concurrent decrease in Cl, Mg, & Ca
Risk factors for Hypokalemia
Age
Alcoholism
Medications
Dietary
Nursing dx for Hypokalemia
- Risk for injury r/t muscle weakness & hyporeflexia
- Ineffective breathing pattern r/t neuromuscular impairment
- decreased cardiac output r/t dysrhythmias
- Constipation r/t smooth muscle atony
- imbalanced nutrition r/t poor dietary levels
- fatigue r/t neuromuscular weakness
Intervention for Hypokalemia
Replacement therapies Diet Supplements- not if UO< 0.5 ml/kg/hr Parenteral Continued monitoring Restoration of balance K sparing diuretics ( spinolactone & triamterene)
Hyperkalemia
> 5.0 mEq/L
Rare w/ normal functioning kidneys
**Myocardium is most sensitive to increase K
Sudden increase shows changed at 6-7 mEq/L
Slow increase shows change at 8 mEq/L
Actual Hyperkalemia
K in ECF is elevated Excessive intake Deceased excretion ( adrenal insufficiency, renal insufficiency/failure, K sparing diuretics, ACE inhibitors)
Relative Hyperkalemia
K moves ICF to ECF Cellular release (burns, trauma) Pseudohyperkalemia- hemolysis Transcellular shifting ( insulin deficiency) Addison's disease (decrease aldosterone)
Clinical manifestation for Hyperkalemia
Cardiovascular-irreg, slow HR, dec BP, ECG
Respiratory- not until very high
Neuromuscular- twitching, cramps, irritable
GI- hypermotility, cramps, N/V/D, weight loss
Assessment for Hyperkalemia
Monitor
Serum K, ECG changes, I&O
Identify risk factors
Age, meds, diet, disease states & therapeutic treatments
Lab findings for Hyperkalemia
K >5.0 mEq/L
If cause is dehydration
Hct, Hgb, Na, Cl
If cause is renal failure
Creatine and BUN also
ABG to monitor for metabolic acidosis
Nursing dx for Hyperkalemia
Risk for injury r/t muscle weakness & seizures
Risk for dec cardiac output r/t dysrhythmias
Imbalance nutrition r/t dec renal function or incr intake
Diarrhea r/t neuromuscular changes & irritability
Interventions for Hyperkalemia
Decrease K intake
Promote K excretion
Monitor
K, s/s Hyperkalemia, cardiac status, metabolic acidosis
Restore balance
Dialysis if Hyperkalemia cannot be controlled in timely manner
Medications for Hyperkalemia
Exchange resins
- kayexalate (Na polystyrene sulfonate) oral or enema
IV
- calcium gluconate
- regular insulin & 50% dextrose
- sodium bicarbonate
Potassium wasting diuretics
Aerosolized beta2 agonist (albuterol)
Calcium
Cause contraction & coagulation & nerve impulses
9.0-10.5mg/dL
Parathyroid hormone & vitamin d control
Bone resorption
Intestinal uptake
Kidney excretion
Normal calcium level
9.0-10.5mg/dL
Calcium in ECF
Protein bound (mostly albumin)
Chelated (citrate,phosphate,sulfate)
Ionized (50% of total)
Free to leave vascular compartment & participate in cellular functions
Hypocalcemia
<9.0mg/dL -little changes have big effect -low serum increases sodium -movement across membrane causing depolarization to occur more easily & inappropriately -acute- life threatening Chronic- body adjusts (osteoporosis)
Causes of Hypocalcemia
Impaired ability to mobilize calcium & bone
Decreased intake or absorption
Abnormal renal losses
Increased protein binding or chelation
Hypocalcemia assessment
- overstimulation of nerves and muscles
- paresthesias to cramps/spasms
- trousseaus signs ( bp cuff makes arm spasm)
- chovsteks sign
- weak thready pulse
- prolonged ST and QT interval
- increased peristalsis
- chronic= bone changes
Hypocalcemia interventions
Drug therapy
Nutrition therapy
Environmental management
Injury prevention
Hypercalcemia
> 10.5mg/dL
- little changes have big effect
- causes excitable
- affected most: heart,muscles,nerves,intestinal smooth muscles
- faster clotting time, inappropriate clots
Hypercalcemia assessment
- first increase hr & bp then decrease
- shortened qt interval, dysrhythmias
- hypertension
- muscle weakness
- altered loc
- decreased peristalsis
- chronic: osteopenia, osteoporosis
Hypercalcemia interventions
Drug therapy
Rehydrate
IV normal saline promotes kidney excretion
Dialysis
Cardiac monitoring
Phosphorus
3.0-4.5mg/dL
Needed for ATP formation
Balanced with calcium
Regulated by parathyroid hormone
Normal phosphorus level
3.0-4.5mg/dL
Hypophosphatemia
<3.0mg/dL
Body effected w/ chronic low levels
Decreased energy metabolism
Increased calcium levels
Hypophosphatemia causes
Malnutrition Antacids Hyperparathyroidism Hyperglycemia (dka) Alcohol abuse Hypercalcemia
Hypophosphatemia assessment
Neuro: ataxia, confusion, seizures
Musculoskeletal: weakness, stiffness, bone pain
Blood disorders: platelet dysfunction, impaired WBC formation
Hypophosphatemia interventions
Drug therapy
IV replacement
Nutrition therapy
Hyperphosphatemia
>4.5mg/dL Increase membrane excitability Coincides with Hypocalcemia Caused by -decreased renal excretion -release from tissue injury -hypoparathyroidism -tumor lysis syndrome
Magnesium
1.8-3.0mg/dL Most stored in bones and cartilage Skeletal muscle contraction CHO metabolism ATP formation Vitamin activation Cell growth Blood coagulation formation
Normal magnesium levels
1.8-3.0mg/dL
Hypomagnesemia
s disease
- medication
Hypomagnesemia assessment
Skeletal muscle weakness Increased impulse transmission -tremors,athetoid movements Tachycardia Hypertension Cardiac arrythmias
Hypomagnesemia interventions
Dc medications: loop diuretics, osmotic diuretics
IV magnesium sulfate
Possibly replace calcium also
Hypermagnesemia
> 3.0mg/dL
Excitable membranes need more stimulus
Caused by increased intake or decreased renal excretion
Hypermagnesemia assessment
Bradycardia, hypotension
Prolonged pr interval w/ widened qrs complex
Drowsy, lethargic
Weak, reduced, reflexes
Hypermagnesemia interventions
Dc all magnesium supplements
If no renal failure
-IV fluids
-loop diuretics
Chloride
98-106mEq/L
- Works w/ Na in ECF
- Formation of hydrochloric acid
- Chloride shift decreases plasma chloride
- Bicarbonate most common exchange
- Imbalance occurs from other electrolyte imbalances
- **Excessive vomiting/prolonged gastric suctioning
Normal chloride levels
98-106mEq/L
