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bsnc 3000 > Fluid & Electrolytes > Flashcards

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)

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2
Q

Consequences of hypokalemia

A

muscle paralysis

respiratory arrest

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3
Q

Cell membrane permeability

A

freely permeable to water

not permeable to electrolytes

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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

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5
Q

What stimulates the thirst center

A

osmoreceptors (detect increased plasma osmolality)
angiotensin II
neurons in the mouth that detect dryness

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6
Q

Fluid Intake

A

ingested fluids
foods –> absorbed in GI tract
metabolic water (~200 mL/daily)

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7
Q

Fluid output

A

kidneys –> urine
GI tract –> feces
skin –> sweat
lungs –> expired air

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8
Q

Diuresis

A

increased water excretion

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9
Q

Natriuresis

A

increased sodium excretion

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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)

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11
Q

Hormones regulating fluid/electrolyte balance

A 
Angiotensin II
Aldosterone*
ADH*
Natriuretic pepties (ANP & BNP)*
Cortisol (mild mineralocorticoid fx)
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12
Q

What stimulates ADH release

A

increased serum osmolality
decreased blood volume/blood pressure
ATII stimulation
stress

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13
Q

Aldosterone mechanism

A

increases insertion of Na+/K+ pumps in the DCT increasing sodium reabsorption
increases potassium excretion

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14
Q

ADH mechanism

A

increases insertion of aquaporin 2 channels in the DCT/collecting duct
causes systemic vasoconstriction

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15
Q

Natriuretic hormone mechanism

A

increase sodium excretion
decrease SNS activity –> inhibit renin release
afferent arteriole vasodilation –> increase GFR (increase diuresis)
vasodilation

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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

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17
Q

Insulin & Potassium

A

insulin increases insertion of Na+/K+ gates –> increases K+ movement into cells

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18
Q

Fluid compartments

A

ICF

ECF

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19
Q

Divisions of ECF

A

intravascular (blood + lymph)

extravascular (interstitial, serous membranes, aqueous humor)

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20
Q

Percentage of K+ stored intracellulary

A

98%

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21
Q

ECV imbalances

A

fluid volume excess –> hypervolemia
fluid volume deficit –> hypovolemia

does not cause a osmotic shift between fluid compartments

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22
Q

Osmolality imbalances

A

hypernatremia –> cellular dehydration
hyponatremia –> cellular swelling

causes osmotic shift between fluid compartments

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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
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24
Q

Common post-op fluid gain

A

IV fluid therapy
feeding tubes
fluid retention d/t PSR (ADH & aldosterone rls)

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25
Q

Common intracellular cations

A

potassium

magnesium

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26
Q

Common intracellular anions

A

phosphate –> usually attached to organic molecules like ATP

proteins

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27
Q

Common extracellular cations

A

sodium

hydrogen

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28
Q

Common extracellular anions

A

bicarbonate

chloride

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29
Q

Sources of sodium intake

A 
processed food
seasoning
medication
canned food 
condiments
canned food
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30
Q

Routes of sodium loss

A

kidneys –> urine
GI –> feces
skin –> sweat (hypotonic)

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31
Q

Na+/K+ pump

A

pumps out 3 sodium from ICF –> ECF
pumps in 2 potassium from ECF –> ICF

*maintains resting membrane potential

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32
Q

Types of hyponatremia

A

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

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33
Q

Normal sodium range (ECF)

A

135-145 mmol/L

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34
Q

Normal potassium range (ICF)

A

3.5-5.0 mmol/L

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35
Q

Causes of hyponatremia

A 
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
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36
Q

Causes of hypernatremia

A

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

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37
Q

Consequences of hyponatremia

A

cerebral edema –> neurologic symptoms (headache, impaired LOC, nerve/motor function, seizures)
peripheral edema

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38
Q

Hyponatremia & cellular excitiability

A

hyponatremia makes depolarization slower = reduced excitability
Na+ needed to cause depolarization

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39
Q

Excitable cells

A

neurons
skeletal muscle fiber
cardiac cells
smooth muscle cells

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40
Q

Resting membrane potential

A

-70 mV

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41
Q

Threshold

A
  • 55 mV

* at this point voltage-gated sodium channels open –> depolarization

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42
Q

Depolarization mV

A

+30 mV

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43
Q

Action potential physiology

A

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

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44
Q

Factors impacting clinical manifestation of hyponatremia

A

underlying cause
acute vs. chronic onset
severity
assoc S/S of fluid gain/loss

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45
Q

Hyponatremia CNS symptoms

A

d/t cerebral edema

fatigue
headache
confusion (altered LOC) 
seizures
coma
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46
Q

Hyponatremia skeletal muscle symptoms

A

muscle weakness
muscle cramps

d/t decreased muscle contractions

47
Q

Hyponatremia GI symptoms

A

nausea

vomiting

48
Q

Hyponatremia CV symptoms

A

hypotension (fluid shift)
tachycardia (SNS activation)
hypovolemic shock

49
Q

S/S of hypovolemia

A 
increased heart rate
decreased blood pressure 
weak, thready pulse
postural hypotension
increased respiratory rate
concentrated urine 
oliguria
50
Q

S/S of hypervolemia

A

edema
dyspnea
weight gain
polyuria

51
Q

Hypernatremia CNS symptoms

A 
fatigue 
headache
confusion 
seizures
coma
52
Q

Hypernatremia cellular dehydration S/S

A 
dry skin & mucous membranes
sunken eyes
decreased skin turgor
hypertension
peripheral edema
53
Q

Hypernatremia compensation

A

increased thirst
oliguria (body wants to hold onto water)
concentrated urine

54
Q

Types of fluid therapy

A 
fluid resuscitation (replacement)
maintenance
55
Q

Purpose of fluid resuscitation

A

replace fluids/electrolytes that have been lost in the body

restore adequate end organ perfusion

56
Q

Purpose of fluid maintenance

A

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
Q

When are S/S of bleeding apparent?

A

after >15% of blood loss

58
Q

Third spacing

A

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
Q

Types of fluid therapies

A

crystalloids –> contain particles that can cross cell membranes
colloids –> large particles cannot cross cell membrane (albumin)
blood products

60
Q

Types of blood products

A

packed red blood cells
fresh, frozen plasma
platelets
cryoprecipitate

61
Q

Types of crystalloid fluids

A

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
Q

Common hypotonic fluids

A

0.45 NaCl (half NS)
D5W
D5 1/2 NS

63
Q

What does dextrose do in plasma?

A

metabolized by cells (sugar) –> pure water remains

64
Q

What does plasma lyte do in plasma

A

metabolizes into acetate –> pure water remains

$$$

65
Q

Common isotonic fluids

A

0.9 NS
Lactated Ringers
Plasmalyte

66
Q

Common hypertonic fluids

A

3-9% NaCl

D20W

67
Q

Purpose of colloid fluids

A

intravascular expanders when blood oncotic pressure is low

common colloid = albumin. expands intravascular volume & prevents fluid from shifting out

68
Q

Treatment of hypovolemic hyponatremia

A

treat underlying condition

normal saline IV

69
Q

Treatment of hypervolemic hyponatremia

A

restrict fluids
diuretics
hypertonic IV fluid if severe –> treat cerebral edema, restore sodium balance

70
Q

Severe hyponatremia

A

acute onset
<120 mmol/L
symptomatic

71
Q

Osmotic demyelination

A

rapid decrease in serum sodium can cause damage to neurons in the brain stem
affects descending pathways –> paralysis, dysarthria, dysphagia

72
Q

Treatment of hypernatremia

A

oral rehydration + treat underlying cause
IV fluids –> isotonic
severe hypernatremia –> hypotonic IV (non-sodium containing fluids)

73
Q

Potassium loss

A

10% lost in feces

most potassium lost in the urine (d/t aldosterone)

74
Q

Potassium & the resting membrane potential

A

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
Q

Causes of hypokalemia

A

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
Q

Causes of hyperkalemia

A

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
Q

B2-adrenergic receptors & potassium

A

increase Na+/K+ pumps
therefore B2 agonists –> hypokalemia (causes potassium to enter cells)
B2 antagonists –> hyperkalemia (inhibit entry of potassium into cells)

78
Q

Alpha adrenergic receptors & potassium

A

increase calcium dependent K+ Channels
alpha antagonists –> hypokalemia
alpha antagonists –> hyperkalemia

79
Q

Hypokalemia & RMP

A

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
Q

GI manifestations of hypokalemia

A

constipation
ileus (decreased motility)
nausea, vomiting

81
Q

Skeletal manifestations of hypokalemia

A

muscle weakness
leg cramps
flaccid paralysis
shallow breathing, respiratory muscle weakness (severe)

82
Q

CV manifestations of hypokalemia

A

ECG changes –> flattened T waves

dysrhythmias

83
Q

Compensation for hypokalemia

A

polyuria (decreased aldosterone rls)

thirst d/t polyuria

84
Q

Hyperkalemia & RMP

A

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
Q

Severe hyperkalemia & RMP

A

sustained subthreshold depolarization –> inactivates sodium channels which decreases excitability

86
Q

GI manifestations of hyperkalemia

A

diarrhea
abdominal cramps
nausea/vomiting

87
Q

Skeletal manifestations of hyperkalemia

A

muscle twitching
muscle weakness
flaccid paralysis (severe)

88
Q

CV manifestations of hyperkalemia

A

ECG changes
bradycardia
cardiac arrest –> ventricular fibrillation

89
Q

Neurologic manifestation of hypokalemia

A

paresthesia

90
Q

When do symptoms of hypokalemia begin?

A

<3.0 mmol

91
Q

When do symptoms of hyperkalemia begin?

A

> 6.0 mmol

rate of increase more important than concentration

92
Q

Treatment for hypokalemia

A

K+ supplements –> oral, IV

93
Q

IV potassium & veins

A

IV potassium irritating to veins
20-40 mEq can be given peripheral IV
>40 mEq requires CVC + cardiac monitoring

94
Q

Treatment for hyperkalemia

A

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
Q

Kayexelate MOA

A

increases fecal K+ excretion

96
Q

Nausea definitoin

A

unpleasant sensation causing an urge to vomit

may or may not vomit

97
Q

Vomiting definition

A

forceful expulsion of upper GI contents thru mouth

98
Q

Vomiting center stimuli

A

vestibular apparatus
cerebral cortex –> memories, thoughts, emotions
GI tract (vagal & glossopharyngeal nerves)
chemoreceptor trigger zone
increased ICP

99
Q

Chemoreceptor trigger zone

A

located in the medulla oblongata outside the blood brain barrier

100
Q

Vomiting & cortex stimuli

A

sensory inputs (pain, smells, sights)
emotions
memories

101
Q

Vomiting & GI tract stimuli

A 
GI distension (bowel obstruction)
GI irritation (gastroenteritis, alcohol, cytotoxic drugs, radiation)
gag reflex

*serotonin, dopamine receptors

102
Q

Vomiting & CTZ stmuli

A

drugs/toxins in blood or CSF
pregnancy hormones

*serotonin, dopamine, opioid receptors

103
Q

Vomiting & Vestibular stimuli

A

motion sickness

*acetylcholine, histamine receptors

104
Q

Retching definition

A

muscular events of vomiting w/o vomit –> dry heaves

105
Q

Regurgitation definition

A

effortless passage of contents into mouth (GERD)

106
Q

PONV Risk Factors

A

female sex
non-smoker
history of PONV
postoperative opioids

107
Q

Other medication w/ anti-emetic fx

A

glucocorticoids
cannabinoids –> chemotherapy pts
benzodiazepines –> adjunct to relieve anxiety/anticipatory emesis

108
Q

Consequences of PONV

A 
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
Q

PONV assessments

A 
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
Q

Non-pharm PONV interventions

A 
raise HOB
cool damp cloth on face/neck
gum chewing
hydration 
isopropyl alcohol swelling
check NG tube for blockage 
acupuncture/acupressure
111
Q

Which anti-emetic does not have sedative fx

A

ondansetron

112
Q

Which anti-emetic can be used for paralytic ileus

A

metoclopramide

113
Q

Nernst equation

A

RMP related to ratio of intracellular to extracellular potassium concentration

intracellular K+ = 150 mmol
extracellular K+ = 3.5-5.0 mmol

114
Q

Consequences of POVN

A 
delayed recovery
risk of aspiration --> pneumonia
wound dehiscence
electrolyte disturbances
dehydration

bsnc 3000 (11 decks)

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