Fluid & Electrolytes Flashcards
Causes of hypokalemia
increased diuresis
GI losses (NG suction, diarrhea, vomiting, laxatives )
insulin (activates Na/K pump)
metabolic/respiratory alkalosis
B2 agonists
hyperaldosteronism
erythropoiesis, leukocytosis, thrombocytosis (K+ stored inside cells)
Consequences of hypokalemia
muscle paralysis
respiratory arrest
Cell membrane permeability
freely permeable to water
not permeable to electrolytes
Where is the thirst center located
In the hypothalamus
*very powerful autonomic reflex –> dehydration is rare unless person is physically or cognitively impaired
What stimulates the thirst center
osmoreceptors (detect increased plasma osmolality)
angiotensin II
neurons in the mouth that detect dryness
Fluid Intake
ingested fluids
foods –> absorbed in GI tract
metabolic water (~200 mL/daily)
Fluid output
kidneys –> urine
GI tract –> feces
skin –> sweat
lungs –> expired air
Diuresis
increased water excretion
Natriuresis
increased sodium excretion
What stimulates renin release
decreased blood pressure
decreased blood volume
stress (B1 adrenergic receptors)
macula densa cells (detect low sodium in the DCT)
Hormones regulating fluid/electrolyte balance
Angiotensin II Aldosterone* ADH* Natriuretic pepties (ANP & BNP)* Cortisol (mild mineralocorticoid fx)
What stimulates ADH release
increased serum osmolality
decreased blood volume/blood pressure
ATII stimulation
stress
Aldosterone mechanism
increases insertion of Na+/K+ pumps in the DCT increasing sodium reabsorption
increases potassium excretion
ADH mechanism
increases insertion of aquaporin 2 channels in the DCT/collecting duct
causes systemic vasoconstriction
Natriuretic hormone mechanism
increase sodium excretion
decrease SNS activity –> inhibit renin release
afferent arteriole vasodilation –> increase GFR (increase diuresis)
vasodilation
Water intoxication
decreased osmolality of plasma causes a fluid shift from ECF –> ICF
cellular swelling –> cellular lysis
cerebral edema –> convulsions, coma, death
Insulin & Potassium
insulin increases insertion of Na+/K+ gates –> increases K+ movement into cells
Fluid compartments
ICF
ECF
Divisions of ECF
intravascular (blood + lymph)
extravascular (interstitial, serous membranes, aqueous humor)
Percentage of K+ stored intracellulary
98%
ECV imbalances
fluid volume excess –> hypervolemia
fluid volume deficit –> hypovolemia
does not cause a osmotic shift between fluid compartments
Osmolality imbalances
hypernatremia –> cellular dehydration
hyponatremia –> cellular swelling
causes osmotic shift between fluid compartments
Common post-op fluid loss
estimated blood loss vomiting diarrhea decreased intake (NPO, N/V, paralytic ileus) fever drainage (NG tube, chest tube, hemovac) intra-op insensible loss (open cavity surgery) new ileostomy
Common post-op fluid gain
IV fluid therapy
feeding tubes
fluid retention d/t PSR (ADH & aldosterone rls)
Common intracellular cations
potassium
magnesium
Common intracellular anions
phosphate –> usually attached to organic molecules like ATP
proteins
Common extracellular cations
sodium
hydrogen
Common extracellular anions
bicarbonate
chloride
Sources of sodium intake
processed food seasoning medication canned food condiments canned food
Routes of sodium loss
kidneys –> urine
GI –> feces
skin –> sweat (hypotonic)
Na+/K+ pump
pumps out 3 sodium from ICF –> ECF
pumps in 2 potassium from ECF –> ICF
*maintains resting membrane potential
Types of hyponatremia
hypovolemia –> water lost in excess of sodium
euvolemia –> water and sodium lost in equal amounts but water restored from ICF or d/t aldosterone/ADH rls
hypervolemia –> sodium lost in excess of water. dilutional hyponatremia
Normal sodium range (ECF)
135-145 mmol/L
Normal potassium range (ICF)
3.5-5.0 mmol/L
Causes of hyponatremia
sodium restricted diet diuretics (thiazide/loop) vomiting, diarrhea, NG suction excess intake of pure water --> dilutional fx conditions causing increased ADH rls --> CHF, cirrhosis, PSR excessive hypotonic IV fluids hyperglycemia (fluid shift) inadequate aldosterone
Causes of hypernatremia
excessive administration of sodium IV fluids (normal saline)
excessive dietary intake
primary hyperaldosteronism
insufficient water intake (dehydration)
increased hypotonic fluid losses –> sweating, RR, watery diarrhea, osmotic diuresis
ADH deficiency, diabetes insipidus
Consequences of hyponatremia
cerebral edema –> neurologic symptoms (headache, impaired LOC, nerve/motor function, seizures)
peripheral edema
Hyponatremia & cellular excitiability
hyponatremia makes depolarization slower = reduced excitability
Na+ needed to cause depolarization
Excitable cells
neurons
skeletal muscle fiber
cardiac cells
smooth muscle cells
Resting membrane potential
-70 mV
Threshold
- 55 mV
* at this point voltage-gated sodium channels open –> depolarization
Depolarization mV
+30 mV
Action potential physiology
1) membrane depolarizes to threshold (-55 mV) causing opening of voltage-gated sodium channels
2) sodium rushes into cell causing cell to reach 0 –> +30 mV
3) repolarization –> potassium exits cell to reestablish RMP
Factors impacting clinical manifestation of hyponatremia
underlying cause
acute vs. chronic onset
severity
assoc S/S of fluid gain/loss
Hyponatremia CNS symptoms
d/t cerebral edema
fatigue headache confusion (altered LOC) seizures coma
Hyponatremia skeletal muscle symptoms
muscle weakness
muscle cramps
d/t decreased muscle contractions
Hyponatremia GI symptoms
nausea
vomiting
Hyponatremia CV symptoms
hypotension (fluid shift)
tachycardia (SNS activation)
hypovolemic shock
S/S of hypovolemia
increased heart rate decreased blood pressure weak, thready pulse postural hypotension increased respiratory rate concentrated urine oliguria
S/S of hypervolemia
edema
dyspnea
weight gain
polyuria
Hypernatremia CNS symptoms
fatigue headache confusion seizures coma
Hypernatremia cellular dehydration S/S
dry skin & mucous membranes sunken eyes decreased skin turgor hypertension peripheral edema
Hypernatremia compensation
increased thirst
oliguria (body wants to hold onto water)
concentrated urine
Types of fluid therapy
fluid resuscitation (replacement) maintenance
Purpose of fluid resuscitation
replace fluids/electrolytes that have been lost in the body
restore adequate end organ perfusion
Purpose of fluid maintenance
TKVO –> to keep vein open
maintain fluid if pt has impaired intake NPO, N/V, ventilator, intra-op, etc.
preventive treatment --> prevent f/e imbalances provide calories (dextrose) to prevent muscle catabolism
When are S/S of bleeding apparent?
after >15% of blood loss
Third spacing
loss of effective circulating blood volume d/t sequestration of fluids in non-functional fluid compartments
ex: ascites, edema, pleural effusion, pericardial effusion, burns
Types of fluid therapies
crystalloids –> contain particles that can cross cell membranes
colloids –> large particles cannot cross cell membrane (albumin)
blood products
Types of blood products
packed red blood cells
fresh, frozen plasma
platelets
cryoprecipitate
Types of crystalloid fluids
isotonic > solute concentration = to blood plasma (used to restore intravascular volume w/o need for fluid shifts)
hypotonic > solute concentration less than blood plasma (used to treat cellular dehydration)
hypertonic > solute concentration greater than blood plasma (used to treat electrolyte deficits, cellular swelling)
Common hypotonic fluids
0.45 NaCl (half NS)
D5W
D5 1/2 NS
What does dextrose do in plasma?
metabolized by cells (sugar) –> pure water remains
What does plasma lyte do in plasma
metabolizes into acetate –> pure water remains
$$$
Common isotonic fluids
0.9 NS
Lactated Ringers
Plasmalyte
Common hypertonic fluids
3-9% NaCl
D20W
Purpose of colloid fluids
intravascular expanders when blood oncotic pressure is low
common colloid = albumin. expands intravascular volume & prevents fluid from shifting out
Treatment of hypovolemic hyponatremia
treat underlying condition
normal saline IV
Treatment of hypervolemic hyponatremia
restrict fluids
diuretics
hypertonic IV fluid if severe –> treat cerebral edema, restore sodium balance
Severe hyponatremia
acute onset
<120 mmol/L
symptomatic
Osmotic demyelination
rapid decrease in serum sodium can cause damage to neurons in the brain stem
affects descending pathways –> paralysis, dysarthria, dysphagia
Treatment of hypernatremia
oral rehydration + treat underlying cause
IV fluids –> isotonic
severe hypernatremia –> hypotonic IV (non-sodium containing fluids)
Potassium loss
10% lost in feces
most potassium lost in the urine (d/t aldosterone)
Potassium & the resting membrane potential
inside of the cell is negative compared to outside of the cell
potassium leak channels –> potassium exits the cell decreasing voltage
ICF contains anions that can’t cross the plasma membrane –> proteins & phosphate bound to organic molecules
maintains negative charge of the RMP
Causes of hypokalemia
reduced dietary intake
excessive K+ free IV fluids
increased loss (vomiting, diarrhea, diuresis, NG suction, laxative abuse)
loop/thiazide diuretics
hyperaldosteronism
B2 agonists, alpha adrenergic antagonists
insulin
alkalosis –> potassium exchanged for hydrogen
Causes of hyperkalemia
increased dietary intake + impaired excretion
rapid infusion of K+ fluids
exercise –> ATP increase Na+/K+ pumps
excessive K+ supplements
hypoaldosteronism
acidosis –> potassium exchanged for hydrogen
blood transfusion (RBC lysis)
medication (ACE-i, ARBs, spironolactone)
kidney disease –> impaired GFR
cellular death (hemolysis, crush injuries, chemotherapy)
B2-adrenergic receptors & potassium
increase Na+/K+ pumps
therefore B2 agonists –> hypokalemia (causes potassium to enter cells)
B2 antagonists –> hyperkalemia (inhibit entry of potassium into cells)
Alpha adrenergic receptors & potassium
increase calcium dependent K+ Channels
alpha antagonists –> hypokalemia
alpha antagonists –> hyperkalemia
Hypokalemia & RMP
makes the RMP more negative
increases concentration gradient causing more intracellular K+ to leave via leak channels
takes LONGER for cells to reach threshold –> slows down cellular metabolism (GI, cardiac, skeletal)
GI manifestations of hypokalemia
constipation
ileus (decreased motility)
nausea, vomiting
Skeletal manifestations of hypokalemia
muscle weakness
leg cramps
flaccid paralysis
shallow breathing, respiratory muscle weakness (severe)
CV manifestations of hypokalemia
ECG changes –> flattened T waves
dysrhythmias
Compensation for hypokalemia
polyuria (decreased aldosterone rls)
thirst d/t polyuria
Hyperkalemia & RMP
hyperkalemia –> changes the concentration gradient inhibiting exit of K+ from inside cell to outside cell
makes the RMP more positive –> cell reaches threshold more easily –> increased depolarization
*increase in cellular activity (GI, cardiac, skeletal)
Severe hyperkalemia & RMP
sustained subthreshold depolarization –> inactivates sodium channels which decreases excitability
GI manifestations of hyperkalemia
diarrhea
abdominal cramps
nausea/vomiting
Skeletal manifestations of hyperkalemia
muscle twitching
muscle weakness
flaccid paralysis (severe)
CV manifestations of hyperkalemia
ECG changes
bradycardia
cardiac arrest –> ventricular fibrillation
Neurologic manifestation of hypokalemia
paresthesia
When do symptoms of hypokalemia begin?
<3.0 mmol
When do symptoms of hyperkalemia begin?
> 6.0 mmol
rate of increase more important than concentration
Treatment for hypokalemia
K+ supplements –> oral, IV
IV potassium & veins
IV potassium irritating to veins
20-40 mEq can be given peripheral IV
>40 mEq requires CVC + cardiac monitoring
Treatment for hyperkalemia
reduce intake –> oral & IV
increase K+ elemination –> kayexalate, diuretics, dialysis (if GFR <15)
insulin + dextrose IV –> cause shift of K+ from ECF to ICF
Kayexelate MOA
increases fecal K+ excretion
Nausea definitoin
unpleasant sensation causing an urge to vomit
may or may not vomit
Vomiting definition
forceful expulsion of upper GI contents thru mouth
Vomiting center stimuli
vestibular apparatus
cerebral cortex –> memories, thoughts, emotions
GI tract (vagal & glossopharyngeal nerves)
chemoreceptor trigger zone
increased ICP
Chemoreceptor trigger zone
located in the medulla oblongata outside the blood brain barrier
Vomiting & cortex stimuli
sensory inputs (pain, smells, sights)
emotions
memories
Vomiting & GI tract stimuli
GI distension (bowel obstruction) GI irritation (gastroenteritis, alcohol, cytotoxic drugs, radiation) gag reflex
*serotonin, dopamine receptors
Vomiting & CTZ stmuli
drugs/toxins in blood or CSF
pregnancy hormones
*serotonin, dopamine, opioid receptors
Vomiting & Vestibular stimuli
motion sickness
*acetylcholine, histamine receptors
Retching definition
muscular events of vomiting w/o vomit –> dry heaves
Regurgitation definition
effortless passage of contents into mouth (GERD)
PONV Risk Factors
female sex
non-smoker
history of PONV
postoperative opioids
Other medication w/ anti-emetic fx
glucocorticoids
cannabinoids –> chemotherapy pts
benzodiazepines –> adjunct to relieve anxiety/anticipatory emesis
Consequences of PONV
discomfort risk for aspiration --> pneumonia wound dehiscence F/E imbalances acid-base imbalance (hydrogen in gastric contents --> alkalosis) impaired nutrition unable to take PO meds
PONV assessments
N/V scale amount, color, consistency onset, frequency, severity medications causing PONV S/S of F/E imbalance lab values GI assessment Pain assessment Nutrition status
Non-pharm PONV interventions
raise HOB cool damp cloth on face/neck gum chewing hydration isopropyl alcohol swelling check NG tube for blockage acupuncture/acupressure
Which anti-emetic does not have sedative fx
ondansetron
Which anti-emetic can be used for paralytic ileus
metoclopramide
Nernst equation
RMP related to ratio of intracellular to extracellular potassium concentration
intracellular K+ = 150 mmol
extracellular K+ = 3.5-5.0 mmol
Consequences of POVN
delayed recovery risk of aspiration --> pneumonia wound dehiscence electrolyte disturbances dehydration
