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GP Final Exam > Fluid & Electrolytes (Part 2) > Flashcards

Fluid & Electrolytes (Part 2) Flashcards

1
Q

Fluid Management Goal

A

Euvolemia

Maintain adequate:
Intravascular fluid volume
LV filling pressure
CO
SBP
Oxygen delivery to tissues

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2
Q

Physical Exam

A

Skin turgor
Mucus membranes
Peripheral pulses
Resting heart rate and blood pressure
Orthostatic changes
Urine output
NPO Status

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3
Q

Body Fluid Composition

A

approx. 55-60% water
2/3 Intracellular
1/3 Extracellular

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4
Q

Functional Compartments
ICF

A

ICF: 40% of your weight
~ 28 L (2/3 of body H20)

Primary Ions:
K+, Mg+2, PO4-2 & proteins

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5
Q

controls constituents of ICF

A

Cell membranes & cellular metabolism

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6
Q

Extracellular fluid
fxn and electrolytes

A

The remaining 1/3 of body water
approx. 20% of body weight

Primarily a Na+, Cl- & NaHCO3 solution

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7
Q

Interstitial Fluid (ISF)

A

surrounds cells
does not circulate
~ 80% of the ECF

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8
Q

Plasma

A

ECF component of blood
~20% of ECF

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9
Q

ECF is 80% ____ & 20% ___.

A

80% interstit.
20% plasma

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10
Q

Examples of extracellular fluid

A

Interstitial Fluid (ISF) (80%)
Plasma (20%)
Transcellular fluid

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11
Q

Transcellular fluid

A

are fluids that are outside of the normal compartments

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12
Q

Transcellular fluids
examples
how many Liters?

A

CSF, digestive (gastric) juices, mucus, etc.

1 - 2 liters of fluid comprise the

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13
Q

Water
values for M, F & obese

A

Total body water (TBW) varies with age, gender & body type

Males: 60%
Females: 50%
Infants: 80%

Obese adults and patients with diabetes generally have less water per kg of body weight

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14
Q

Basic constituent of the human body

A

water

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15
Q

Laboratory Evaluation
Hypovolemia

A

Increasing Hct
Metabolic acidosis (severe hypovolemia)
Urine SG >1.010
Urine Na < 10 mEq/L
Urine osmolality > 450 mOsm/kg
Hypernatremia
BUN: creatinine ratio > 10:1

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16
Q

Urine specific gravity assessment

A
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17
Q

Signs of Hypovolemia
5%
10%
15-20%

A
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18
Q

⭐️
Hypovolemia
A drop in BP does not occur in a patient that is already in the supine position until about __% of the blood volume is lost

A

30

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19
Q

Intraop Urine output goals

A

0.5-1 ml/kg/hr

BURN pts:
1.5 ml/kg/hr

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20
Q

Decrease in urine output generally does not occur until ___% of blood volume is lost

A

~20

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21
Q

Hypervolemia
What would we see in a CXR?
What labs should we draw?

A

Kerly B lines: Increased pulmonary & interstitial markings

Diffuse alveolar infiltrates

Labs: blood & UA

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21
Q

Signs of Hypervolemia

A

Pitting edema
Presacral edema

Later signs:
Tachycardia
Crackles
Wheezing
Pulmonary edema

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22
Q

T/F
Chest X-ray is not a reliable assessment tool for hypervolemia.

A

False

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23
Q

Electrolytes
ECF & ICF

A

ECF:
Major (+): Na, K, Ca
Major (-): Cl, Bicarb, Proteins

ICF:
Major (+): Na, K, Mag
Major (-): Cl, Bicarb, Proteins

*same major anions
*difference is in major cations
“this is Ma Mag”
“Kick out Ca”

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24
Q

Most important electrolytes

A

Sodium, Potassium, and Calcium

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25
Q

affects resting membrane potential

A

K

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26
Q

determines threshold potential

A

Ca

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27
Q

Na fxn

A

resting potential
generate & propagate AP

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28
Q

Which ions affect excitability of nerve & muscle?

A

Sodium, Potassium, and Calcium

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29
Q

He didn’t emphasize this chart much

A
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30
Q

Hypernatremia
cause
at risk population

A

Secondary to lack of water

At risk:
Debilitated and dehydrated
Extremes of age
Altered LOC

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31
Q

T/F
Hypernatremia is often d/t excessive sodium intake

A

False
Secondary to lack of water – not because of too much salt

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32
Q

HyperNa
S/S

A

S/S:
Restlessness, lethargy, seizures and death

-reflect rate of H20 movement from brain
-Ruptured cerebral veins, focal hemorrhage

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33
Q

Na NR

A

135 - 145 mEq/L

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34
Q

Most common cause of diabetes insipidus

A

Hypernatremia
in a pt that normally has no Na imbalance
(normal total body sodium)
results from medical intervention

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35
Q

diabetes insipidus
w/ normal total body sodium

A

↓↓↓ renal “concentrating-ability”
↓ ADH secretion
renal tubules don’t respond normally to circulating ADH (polyuria)

polyuria
excessive pale urine

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36
Q

⭐️
HyperNa w/ low total body Na

A

Lost sodium & water
Water loss > sodium loss

Losses:
renal (osmotic diuresis)
or
extrarenal (diarrhea or sweat)

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37
Q

⭐️
HyperNa w/ increased total body sodium

A

Most commonly caused by the administration of large quantities of hypertonic Na+ solutions (3% NaCl or 7.5% NaHCO3)

Cushing’s syndrome – too much ACTH

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38
Q

hypertonic Na+ solutions

A

3% NaCl or 7.5% NaHCO3

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39
Q

⭐️
Most commonly caused by the administration of large quantities of hypertonic Na+ solutions

A

HyperNa w/ increased total body Na

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40
Q

Cushing’s syndrome = too much ___

A

ACTH

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41
Q

Hypernatremia > 145 mEq/L
S/S

A

Neuro:
Extreme Thirst
Progressive Weakness & Fatigue
Intracranial bleeding (brain shrinks→vessels pull/shear)
Disorientation, Hallucination, Irritability

CV:
Hypovolemia

Renal:
Oliguria
Renal Insufficiency

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42
Q

⭐️
Treatment of Hypernatremia
how fast can we correct it?

A

fluid deficits corrected over 48 - 72 hours:
hypotonic solution (D5W)

MAX Na decrease: 0.5 - mEq/L/hour

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43
Q

Rapid fluid deficit correction can result in

A

seizure, cerebral edema and coma

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44
Q

Elective surgery should be postponed until sodium level is ___ mEq/L and H2O deficits corrected

A

< 150

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45
Q

Hyponatremia
a/w:

A

alcoholism
liver failure
severe burns
malignant neoplasms
hemodialysis and sepsis

46
Q

⭐️
Na
Neurologic symptoms occur below…

A

120 mEq/L

47
Q

Hyponatremia is serum Na of…

A

< 135 mEq/L

48
Q

Hyponatremia
S/S

A

Neurological:
Seizures → Coma
Cerebral edema
Agitation, Confusion, h/a

GI:
N/V → anorexia

Musculoskeletal: cramps and weakness

May not see when under GA!

49
Q

Hyponatremia
Diagnosis is based on the assessment of:

A

serum osmolality
volume status

50
Q

Osmolality & Osmolarity

A

Osmolality: number of osmoles of solute per kilogram of water (e.g., weight)

Osmolarity: number of osmoles of solute per liter of water (e.g. fluid)

51
Q

Tonicity

A

Effect a solution has on cell volume

Hypertonic
Hypotonic
Isotonic

52
Q

Osmosis is movement of ___

A

H20

53
Q

Plasma Osmolarity
NR and equation

A
54
Q

Plasma Osmolarity
Most important determinant

A

Na+

55
Q

What increases plasma osmolarity?

A

Hyperglycemia or high BUN

56
Q

⭐️
Normal Osmolality

A

280 – 295 mOsm/kg

57
Q

H20 flows from compartment of low to high (osmolarity/osmolality) if the membrane between the compartments is permeable to H2O

A

osmolality

(a cell in relatively hyperosmolar solution: fluid moves out of cell → highly [ ] compartment to reach homeostasis →→ cell shrinks)

58
Q

Osmolality
Reflects fluid shifts from ….
what happens to Na?

A

ICF → ECF
Decreased plasma sodium levels

59
Q

Meds that can change normal plasma osmolality

A

amitriptyline
cyclophosphamides
Tegretol
morphine

60
Q

Disease processes that can shift fluid from ICF → ECF

A

hypothyroidism,
glucocorticoid insufficiency
SIADH

61
Q

SIADH
(inappropriate antidiuretic secretion)
clinical presentation

A

Clinically euvolemic & good renal fxn!
but
↑ urine osmolality (>200mOsm) WITH ↓ serum osmolality

Urine Na >20 mEq/L

62
Q

Causes of SIADH
Dz & Rx

A

Pulmonary carcinoma
Brain metastases, other malignancies
CNS disorders
Idiopathic forms – esp old ppl

Meds:
antidepressants agents (SSRIs)
HCTZ
NSAIDs
Vincristine (chemo for leukemia & others)
Neuroleptic agents
Haldol (PONV; D2 receptor antag in CTZ)
Zyprexa (ADHD)
Vasopressin
Oxytocin

63
Q

⭐️
SIADH Acute treatment starts @ Na levels of ____.

A

<110 (SEVERE hypoNa)

64
Q

SIADH Acute treatment
interventions

A

(Na <110)

IV Lasix – diuresis
NS with 20–40 mEq/L KCL

65
Q

⭐️
Can we use 3% NS for Acute SIADH? Why or why not?

A

Rare
replacement MUST be done slowly, over days
risk: central pontine myelinolysis (demyelinate brain’s white matter)
↓
quadraplegia

66
Q

SIADH (Chronic treatment)

A

-Water restriction ~1000 ml QD
-Declomycin – mechanism unknown
-Urea
-PO Salt tablets
-Vasopressin receptor antagonists:
Conivaptan, Vaprisol, Tolvaptan, Samsca
Lithuim

67
Q

HypoNa in HYPERtonic state

A

pt has high osmolality (>295 mOsm /kg)

Hypervolemia caused by:
Mannitol excess
Glycerol Treatment
Nephrotic Syndrome
CHF
Cirrhosis

Treatment:
Salt/water restriction or diuretics

68
Q

HypoNa in a Hypotonic state

A

Low serum osmolality (<280 mOsm/kg)

assess volume status
hypovolemia may be due to:
-GI losses
-Renal losses + excess water ingestion
-Diuretics
-ketonuria
-3rd Spacing
-adrenal insufficiency
-N & V

69
Q

⭐️
Hyponatremia
How fast do we correct it?

A

Not too fast!
Pontine myelinolysis risk permanent damage!

70
Q

Pontine myelinolysis
S/S

A

Balance problems
Confusion/delirium/∆s in consciousness
dysphagia
Hallucinations
speech changes/poor enunciation
Tremors
weakness face, arms, or legs; usually B/L
Acute progressive quadriplegia

71
Q

HypoNa Tx

A

symptomatic: consider 3% NaCl
sodium 1-2 mEq/L/hr x 2H →0.5 mEq /L/hr

asymptomatic: sodium 0.5 mEq/L/hr

Max in 24 hr: 10 mEq TOTAL rise
Max in 48 hr: 18 mEq TOTAL rise

72
Q

HypoNa Tx
MAX rise in Na over 24 & 48 H

A

Max in 24 hr: 10 mEq TOTAL rise
Max in 48 hr: 18 mEq TOTAL rise

73
Q

Potassium
NR

A

3.0 – 5.5 mEq

74
Q

Hyperkalemia results in altered distribution between…

A

Altered distribution of K between intra- & extracellular sites

75
Q

HyperK
Adverse effects are d/t…

A

to acute ↑ in serum concentration

76
Q

HyperK
Most detrimental effect occurs in….
What do we see?

A

cardiac conduction system

Prolonged PR interval
Widening QRS complex
Peaked T wave

77
Q

Hyperkalemia is serum K greater than….

A

5.5

78
Q

HyperK
causes & S/S

A
79
Q

Treatment of Hyperkalemia

A

-NaHCO3 (~50 mEq) ↑cell uptake of K+ w/in 15 minutes (Note: cannot be used alone)

-Beta agonists
-Glucose 30-50 gm + Insulin 10 units (can take up to 1 hour)
-Hyperventilation
-dialysis
-Ca (cont on another card)

80
Q

Treatment of Hyperkalemia
Ca

A

protect 🩷 from hyperK (1 amp = 1 gm CaCl)

↓ excitability & threshold potential

500-1000 mg IV: antag 🩷 effects; rapid but short-lived

⚠️Ca potentiates digoxin toxicity

81
Q

Ca potentiates ____ toxicity

A

Digoxin

82
Q

Hyperkalemia
Tx algorithm

A
83
Q

HyperK vs HypoK
ECG changes

A

HYPER:
Prolonged PR interval
Widening QRS complex
Peaked T wave

HYPO:
Flattened T waves and presence of U wave

84
Q

How does pH affect K?

A

(indirectly proportional relationship)

0.1 change in arterial pH = 0.6 meq change plasma K+

Acidosis:
-high Plasma K in relation to total body stores
-K depletion d/t urinary or GI losses: plasma concentration may be normal or reduced

85
Q

The bajillion causes of hypoK

A
86
Q

Treatment of Hypokalemia

A

PO KCL 60-80 mEq/day (sour tummy common)

IV:
Peripheral: MAX 8 mEq/hr (vein irritation)
Central: 10-20 mEq/hr

87
Q

What K values do we need to proceed with surgery?

A

greater than 3-3.5mEq/L

88
Q

(hypo/hyper)kalemia causes increased sensitivity to NMBs. So we should decrease the dose by ___%

A

hypoK
25-50%

89
Q

Ca NR

A

8.5-10.5 mg/dl

90
Q

Hypocalcemia
is a/w…

A

hypoparathyroid
pancreatitis
renal failure
decreased albumin

91
Q

HypoCa
affects on muscle

A

Skeletal muscle spasm including laryngospasm

↓ 🩷 contractility

⚠️ Avoid Hyperventilation
pH 0.1 increase (alkalosis) = 0.16 mg/dL decrease ionized Ca

92
Q

What should we avoid with hypoCa?

A

⚠️ Avoid Hyperventilation

pH 0.1 increase (alkalosis) = 0.16 mg/dL decrease ionized Ca

93
Q

Hypocalcemia
EKG changes

A

Mild: broad-based tall peaking T waves

Severe: extremely wide QRS, low R wave, no p waves, tall peaking T waves

94
Q

Hypocalcemia
S/S

A

HTN before hypovolemia (usually)
Anorexia, N/V
Weakness, muscle aches, tingling lips
Muscle spasms of the throat (laryngospasm)
Polyuria
Ataxia
Irritability, lethargy, or confusion
Seizures, Coma → Death

*Trousseau’s Sign: BP cuff = carpopedal spasm
*Chvosteks’s Sign: tap facial CN; edge of mouth spasms

95
Q

Trousseau’s & Chvostek’s sign are a/w

A

HypoCa

96
Q

Treatment of Hypocalcemia

A

Symptomatic = true medical emergency

Rule of 10’s:
10mL 10% calcium gluconate/Cl over 10 mins
↓
drip: elemental calcium 0.3-2 mg/kg/hr

serial ionized Ca

Check magnesium and consider giving magnesium 1 gm

97
Q

Which is a/w necrosis?
Ca gluconate
CaCl

A

CaCl

(Ca gluconate is better for periph IV)

98
Q

When correcting hypoCa, what other electrolyte should we gve?

A

Check magnesium
consider magnesium 1 gm

99
Q

Hypercalcemia
ranges

A

Serum Ca+ > 10.5

ionized >5.6 mg/dL

100
Q

HyperCa
causes

A

Hyperparathyroidism
Malignancy - bone
Renal Failure
Thiazide Diuretics
Excess Ca+ supplements

101
Q

HyperCa
S/S

A

HTN
Dysrhythmias →CHB
Shortened QT
Sedation
Polyuria
Anorexia
Pancreatitis

102
Q

Treatment of Hypercalcemia

A

1) Rehydrate w/ NS
2) brisk diuresis (200-300 ml/hr)
*loop diuretic to ↑Ca excretion
3) serial ionized calcium

Avoid acidosis may further elevate calcium levels

103
Q

How does pH affect Ca?

A

Acidosis can further elevate Ca

104
Q

Magnesium
NR

A

1.7 – 2.2

105
Q

Low Magnesium
causes

A

Alcoholism
Chronic diarrhea
polyuria
sweating
Hyperaldosteronism
Malnutrition
Malabsorption syndromes (celiac, IBS)

meds:
diuretics
aminoglycoside antibiotics
chemotherapy

106
Q

Symptoms: Hypomagnesemia

A

Abnormal eye movements (nystagmus)
Seizure
Fatigue
Muscle spasms or cramps
Muscle weakness
Numbness
Dysrhythmias

107
Q

Treatment of Hypomagnesemia

A

IV mag sulfate 1-2 G slowly over 60 minutes

-Assess for concomitant hypoK or hypoCa

-Monitor EKG for arrhythmias
(Identical to hypokalemia: Flattened T waves and presence of U wave)

108
Q

HypoMg shows the same EKG abnormalities as ….

A

hypoK
Flattened T waves and presence of U wave

109
Q

Hypomag is often accompanied by which other ‘lyte imbalances?

A

hypoK or hypoCa

110
Q

Hypermagnesemia
S/S

A

Flushing
Nausea & vomiting
Drowsiness
Weakness
Loss of patellar reflex, decreased DTRs
Respiratory depression
Cardiac arrest
Coma

111
Q

Treatment of Hypermagnesemia

A

Stop all sources of magnesium

-IV Ca 1G (temporarily antagonize most effects)
-Loop diuretic + rehydration D1/2 NS (enhances excretion)

-Monitor for vasodilation and negative inotropic effects

-Decrease dosages of NDMB by 25-50%

112
Q

Hypermag
anesthesia considerations

A

Decrease dosages of NDMB by 25-50%

(hypoK: decrease NMB dose 25-50%)

GP Final Exam (3 decks)

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