Fluid & Electrolytes Flashcards
1
Q
Causes of hypokalemia
A
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)
2
Q
Consequences of hypokalemia
A
muscle paralysis
respiratory arrest
3
Q
Cell membrane permeability
A
freely permeable to water
not permeable to electrolytes
4
Q
Where is the thirst center located
A
In the hypothalamus
*very powerful autonomic reflex –> dehydration is rare unless person is physically or cognitively impaired
5
Q
What stimulates the thirst center
A
osmoreceptors (detect increased plasma osmolality)
angiotensin II
neurons in the mouth that detect dryness
6
Q
Fluid Intake
A
ingested fluids
foods –> absorbed in GI tract
metabolic water (~200 mL/daily)
7
Q
Fluid output
A
kidneys –> urine
GI tract –> feces
skin –> sweat
lungs –> expired air
8
Q
Diuresis
A
increased water excretion
9
Q
Natriuresis
A
increased sodium excretion
10
Q
What stimulates renin release
A
decreased blood pressure
decreased blood volume
stress (B1 adrenergic receptors)
macula densa cells (detect low sodium in the DCT)
11
Q
Hormones regulating fluid/electrolyte balance
A
Angiotensin II Aldosterone* ADH* Natriuretic pepties (ANP & BNP)* Cortisol (mild mineralocorticoid fx)
12
Q
What stimulates ADH release
A
increased serum osmolality
decreased blood volume/blood pressure
ATII stimulation
stress
13
Q
Aldosterone mechanism
A
increases insertion of Na+/K+ pumps in the DCT increasing sodium reabsorption
increases potassium excretion
14
Q
ADH mechanism
A
increases insertion of aquaporin 2 channels in the DCT/collecting duct
causes systemic vasoconstriction
15
Q
Natriuretic hormone mechanism
A
increase sodium excretion
decrease SNS activity –> inhibit renin release
afferent arteriole vasodilation –> increase GFR (increase diuresis)
vasodilation
16
Q
Water intoxication
A
decreased osmolality of plasma causes a fluid shift from ECF –> ICF
cellular swelling –> cellular lysis
cerebral edema –> convulsions, coma, death
17
Q
Insulin & Potassium
A
insulin increases insertion of Na+/K+ gates –> increases K+ movement into cells
18
Q
Fluid compartments
A
ICF
ECF
19
Q
Divisions of ECF
A
intravascular (blood + lymph)
extravascular (interstitial, serous membranes, aqueous humor)
20
Q
Percentage of K+ stored intracellulary
A
98%
21
Q
ECV imbalances
A
fluid volume excess –> hypervolemia
fluid volume deficit –> hypovolemia
does not cause a osmotic shift between fluid compartments
22
Q
Osmolality imbalances
A
hypernatremia –> cellular dehydration
hyponatremia –> cellular swelling
causes osmotic shift between fluid compartments
23
Q
Common post-op fluid loss
A
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
24
Q
Common post-op fluid gain
A
IV fluid therapy
feeding tubes
fluid retention d/t PSR (ADH & aldosterone rls)
25
Common intracellular cations
potassium
| magnesium
26
Common intracellular anions
phosphate --> usually attached to organic molecules like ATP
| proteins
27
Common extracellular cations
sodium
| hydrogen
28
Common extracellular anions
bicarbonate
| chloride
29
Sources of sodium intake
```
processed food
seasoning
medication
canned food
condiments
canned food
```
30
Routes of sodium loss
kidneys --> urine
GI --> feces
skin --> sweat (hypotonic)
31
Na+/K+ pump
pumps out 3 sodium from ICF --> ECF
pumps in 2 potassium from ECF --> ICF
*maintains resting membrane potential
32
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
33
Normal sodium range (ECF)
135-145 mmol/L
34
Normal potassium range (ICF)
3.5-5.0 mmol/L
35
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
```
36
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
37
Consequences of hyponatremia
cerebral edema --> neurologic symptoms (headache, impaired LOC, nerve/motor function, seizures)
peripheral edema
38
Hyponatremia & cellular excitiability
hyponatremia makes depolarization slower = reduced excitability
Na+ needed to cause depolarization
39
Excitable cells
neurons
skeletal muscle fiber
cardiac cells
smooth muscle cells
40
Resting membrane potential
-70 mV
41
Threshold
- 55 mV
| * at this point voltage-gated sodium channels open --> depolarization
42
Depolarization mV
+30 mV
43
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
44
Factors impacting clinical manifestation of hyponatremia
underlying cause
acute vs. chronic onset
severity
assoc S/S of fluid gain/loss
45
Hyponatremia CNS symptoms
d/t cerebral edema
```
fatigue
headache
confusion (altered LOC)
seizures
coma
```
46
Hyponatremia skeletal muscle symptoms
muscle weakness
muscle cramps
d/t decreased muscle contractions
47
Hyponatremia GI symptoms
nausea
| vomiting
48
Hyponatremia CV symptoms
hypotension (fluid shift)
tachycardia (SNS activation)
hypovolemic shock
49
S/S of hypovolemia
```
increased heart rate
decreased blood pressure
weak, thready pulse
postural hypotension
increased respiratory rate
concentrated urine
oliguria
```
50
S/S of hypervolemia
edema
dyspnea
weight gain
polyuria
51
Hypernatremia CNS symptoms
```
fatigue
headache
confusion
seizures
coma
```
52
Hypernatremia cellular dehydration S/S
```
dry skin & mucous membranes
sunken eyes
decreased skin turgor
hypertension
peripheral edema
```
53
Hypernatremia compensation
increased thirst
oliguria (body wants to hold onto water)
concentrated urine
54
Types of fluid therapy
```
fluid resuscitation (replacement)
maintenance
```
55
Purpose of fluid resuscitation
replace fluids/electrolytes that have been lost in the body
| restore adequate end organ perfusion
56
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
```
57
When are S/S of bleeding apparent?
after >15% of blood loss
58
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
59
Types of fluid therapies
crystalloids --> contain particles that can cross cell membranes
colloids --> large particles cannot cross cell membrane (albumin)
blood products
60
Types of blood products
packed red blood cells
fresh, frozen plasma
platelets
cryoprecipitate
61
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)
62
Common hypotonic fluids
0.45 NaCl (half NS)
D5W
D5 1/2 NS
63
What does dextrose do in plasma?
metabolized by cells (sugar) --> pure water remains
64
What does plasma lyte do in plasma
metabolizes into acetate --> pure water remains
| $$$
65
Common isotonic fluids
0.9 NS
Lactated Ringers
Plasmalyte
66
Common hypertonic fluids
3-9% NaCl
| D20W
67
Purpose of colloid fluids
intravascular expanders when blood oncotic pressure is low
| common colloid = albumin. expands intravascular volume & prevents fluid from shifting out
68
Treatment of hypovolemic hyponatremia
treat underlying condition
| normal saline IV
69
Treatment of hypervolemic hyponatremia
restrict fluids
diuretics
hypertonic IV fluid if severe --> treat cerebral edema, restore sodium balance
70
Severe hyponatremia
acute onset
<120 mmol/L
symptomatic
71
Osmotic demyelination
rapid decrease in serum sodium can cause damage to neurons in the brain stem
affects descending pathways --> paralysis, dysarthria, dysphagia
72
Treatment of hypernatremia
oral rehydration + treat underlying cause
IV fluids --> isotonic
severe hypernatremia --> hypotonic IV (non-sodium containing fluids)
73
Potassium loss
10% lost in feces
| most potassium lost in the urine (d/t aldosterone)
74
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
75
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
76
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)
77
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)
78
Alpha adrenergic receptors & potassium
increase calcium dependent K+ Channels
alpha antagonists --> hypokalemia
alpha antagonists --> hyperkalemia
79
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)
80
GI manifestations of hypokalemia
constipation
ileus (decreased motility)
nausea, vomiting
81
Skeletal manifestations of hypokalemia
muscle weakness
leg cramps
flaccid paralysis
shallow breathing, respiratory muscle weakness (severe)
82
CV manifestations of hypokalemia
ECG changes --> flattened T waves
| dysrhythmias
83
Compensation for hypokalemia
polyuria (decreased aldosterone rls)
| thirst d/t polyuria
84
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)
85
Severe hyperkalemia & RMP
sustained subthreshold depolarization --> inactivates sodium channels which decreases excitability
86
GI manifestations of hyperkalemia
diarrhea
abdominal cramps
nausea/vomiting
87
Skeletal manifestations of hyperkalemia
muscle twitching
muscle weakness
flaccid paralysis (severe)
88
CV manifestations of hyperkalemia
ECG changes
bradycardia
cardiac arrest --> ventricular fibrillation
89
Neurologic manifestation of hypokalemia
paresthesia
90
When do symptoms of hypokalemia begin?
<3.0 mmol
91
When do symptoms of hyperkalemia begin?
>6.0 mmol
| rate of increase more important than concentration
92
Treatment for hypokalemia
K+ supplements --> oral, IV
93
IV potassium & veins
IV potassium irritating to veins
20-40 mEq can be given peripheral IV
>40 mEq requires CVC + cardiac monitoring
94
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
95
Kayexelate MOA
increases fecal K+ excretion
96
Nausea definitoin
unpleasant sensation causing an urge to vomit
| may or may not vomit
97
Vomiting definition
forceful expulsion of upper GI contents thru mouth
98
Vomiting center stimuli
vestibular apparatus
cerebral cortex --> memories, thoughts, emotions
GI tract (vagal & glossopharyngeal nerves)
chemoreceptor trigger zone
increased ICP
99
Chemoreceptor trigger zone
located in the medulla oblongata outside the blood brain barrier
100
Vomiting & cortex stimuli
sensory inputs (pain, smells, sights)
emotions
memories
101
Vomiting & GI tract stimuli
```
GI distension (bowel obstruction)
GI irritation (gastroenteritis, alcohol, cytotoxic drugs, radiation)
gag reflex
```
*serotonin, dopamine receptors
102
Vomiting & CTZ stmuli
drugs/toxins in blood or CSF
pregnancy hormones
*serotonin, dopamine, opioid receptors
103
Vomiting & Vestibular stimuli
motion sickness
*acetylcholine, histamine receptors
104
Retching definition
muscular events of vomiting w/o vomit --> dry heaves
105
Regurgitation definition
effortless passage of contents into mouth (GERD)
106
PONV Risk Factors
female sex
non-smoker
history of PONV
postoperative opioids
107
Other medication w/ anti-emetic fx
glucocorticoids
cannabinoids --> chemotherapy pts
benzodiazepines --> adjunct to relieve anxiety/anticipatory emesis
108
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
```
109
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
```
110
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
```
111
Which anti-emetic does not have sedative fx
ondansetron
112
Which anti-emetic can be used for paralytic ileus
metoclopramide
113
Nernst equation
RMP related to ratio of intracellular to extracellular potassium concentration
intracellular K+ = 150 mmol
extracellular K+ = 3.5-5.0 mmol
114
Consequences of POVN
```
delayed recovery
risk of aspiration --> pneumonia
wound dehiscence
electrolyte disturbances
dehydration
```
