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Flashcards in Electrolytes Deck (82)
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1
Q

Isotonic contraction

A
Equal sodium and water loss
Vomiting. diarrhea
Kidney disease, diuretics
Cholera
Replace with NS
2
Q

Normal Na+ and osmolality

A

135-145 mEq/L

280-300 mOsm/kg

3
Q

Hypertonic contraction

A

More water than Na+ loss.
Extracellular hypertonicity draws water out of cells, partially compensating for loss of volume
Sweating, excessively concentrated baby food, burns, unable to respond to thirst
Hypertonic contraction tx with hypotonic saline
Replace 50% of volume in first few hours, rest over 1-2 days

4
Q

Hypotonic contraction

A

More Na+ than water loss
Volume and osmolality of ECF are reduced, which moves ECF into cells.
Usually from excess Na+ lost through kidneys from insufficiency, hypoaldosteronism, diuretics.

5
Q

Hypervolemic hyponatremic volume expansion

A

Vasopressin antagonist (conivaptan, tolvaptan)

6
Q

Acid-base status regulation

A

Bicarb-carbonic acid buffer
Respiratory system
Kidneys

7
Q

Acid base

A

CO2 represents volatile carbonic acid, exhalation of CO2 tends to elevate pH (reduce acidity)
Kidneys raise pH by retaining bicarb or lower by excreting

8
Q

Respiratory alkalosis

A

Hyperventilation blows off too much Co2 which lowers pCO2 and increases pH.
Tx by rebreathing CO2, giving 5% CO2 or giving a sedative

9
Q

Respiratory acidosis

A

CO2 retention from hypoventilation which raises pCO2 causing pH to fall. Hypoventilation or air trapping.

10
Q

Metabolic Alkalosis

A

Increase in pH and bicarb. Vomiting, suctioning, alkalinizing salts.
Body corrects with hypoventilation and increased renal bicarb excretion.
Sodium chloride plus potassium chloride facilitates renal excretion of bicarb and promotes normalization of plasma pH.

11
Q

Metabolic Acidosis

A

Chronic renal failure, diarrhea, lactic acidosis or ketoacidosis. Methanol, ASA.
Bicarb

12
Q

Intracellular K+

A

150mEq/L.
Most abundant intracellular cation.
Extracellular 4-5mEq/L
Nerve impulses and acid/base balance

13
Q

Potassium regulation

A

Excretion increased by aldosterone which increases Na+ reabsorption

14
Q

Hypokalemia

A

Less than 3.5 mEq/L
Thiazide or loop diuretic
Insufficient intake, alkalosis, excessive insulin, excess aldosterone, vomiting, diarrhea and laxatives can all cause hypokalemia.
Weakness, paralysis, dysrhythmias, intestinal dilation and ileus.
Principal cause of dig tox
Risk of HTN and stroke

15
Q

HypoK+ TX

A

Potassium Chloride preferred as chloride deficiency goes with hypoK
Oral may upset GI tract
Take with meals to decrease chance of localized hyper K resulting in severe intestinal injury.

16
Q

Potassium IV dilution

A

40mEq/L or less

Monitor ECG changes

17
Q

HyperK+ causes

A

Severe tissue trauma, addison’s disease, acute acidosis, acute renal failure, misuses of K+ sparing diuretics, OD with IV K+

18
Q

Kayexalate, kionex

A

An exchange resin that absorbs potassium

19
Q

Mag needed for

A

Activity of many enzymes and binding of mRNA to ribosomes.
Also neurochemical transmission and muscle excitability
40 mEq/L intracellularly
2mEq/L extra

20
Q

Hypomag causes and consequence

A

Diarrhea, hemodialysis, kidney disease, prolonged IV feeding with mag free solutions, ETOH abuse, diabetes, pancreatitis.
Often goes with hypocalcemia and hypokalemia

21
Q

Hypomag symptoms

A

Ach at NMJ is enhances, increasing muscle excitability to the point of tetany.
Increases excitability of neurons causing disorentation, psychoses and seizures
May cause calcium stones in nephrons

22
Q

Excess mag

A

Neuromuscular blockade resulting in paralysis of resp muscles (12-15 mEq/L, at 25 cardiac arrest).
Can intensify effects of NMBAs and can be countered with calcium
Contraindicated with heart blocks as it may suppres AV impulse conduction

23
Q

Symptoms of excess mag

A

Muscle weakness from inhibition of Ach, hypotension, sedation, ECG changes.

24
Q

HyperK causes

A
K+ sparing diuretics
ACE inhibitors 
NSAIDS
Renal
Rhabdo
Acidosis (renal, diarrhea, DKA, ASA)
Hemolysis
Diet
ADdisons
25
Q

Hyper K presentation

A
Cardiac
N/V
Diarrhea
Muscular weakness
Dysrhythmias
26
Q

Tented T waves

A

5.5-6

27
Q

Normal K+

A

3.5-5

28
Q

PR/QT prolongation K+

A

6-6.5

29
Q

6.5-7 K+

A

Flat P/ST segment

30
Q

7-7.5 K+

A

QRS widening

31
Q

ST merging K+

A

7.5-8 mEq

32
Q

Sine wave/IVR K+

A

8-10

33
Q

> 10 K+

A

VT/VF

34
Q

TX for mild hyper K (5-6mEq)

A

Lasix 1mg/kg SIVP
Kayexalate
Dialysis

35
Q

Moderate hyper K TX (6-7)

A

Bicarb 50mEq over 5 minutes
Glucose + slin 50g D50 plus 10 IU regular insulin over 15-30 minutes
Ventol 15mg over 15 minutes

36
Q

K+ TX over 7 (severe)

A

10mL of 10% solution over 10 minutes (1g)
8-16mg/kg no faster than 100mg/min
Bicarb

37
Q

Plasma buffering bicarb formulation

A

HCO3+ + H+ = H2CO3 = H2O + CO2

38
Q

Pharmacokinetics of bicarb

A

8.4 solution (4.2 in Peds)
1mmol Na+ and 1mmol HCO3 per mL
pH = 7.8

39
Q

Bicarb uses

A

Prolonged cardiac arrest
Hyper K
Metabolic acidosis
Cocaine, TCA, ASA OD

40
Q

Adverse effects/contras of bicarb

A

Alkalosis, hypernatremia, extravasation causes significant damage
Contras are arrest without a tube, hypernatremia, alkalosis

41
Q

Precautions of bicarb

A
Monitor labs
Hypocalcemia (tetany)
Excessive chloride loss from vomiting or GI suction
Hypokalemia
Renal or heart failure
42
Q

Bicarb doses

A

Arrest and OD 1mEq/kg SIVP
Repeat the dose once for OD
HyperK 50 mEq

43
Q

Kayexolate

A

Sodium Polystyrene Sulfonate

Class is cation-exchange resin

44
Q

Kayexolate MOA

A

Cation exchange system in GI tract is utilized, it donates Na+ ion which causes K+ excretion in GI tract where kayexolate binds to K+ to remove through GI

45
Q

Adverse effects of kayexolate

A

Fecal impaction constipation
N/V
Lyte issues
Colonic necrosis

46
Q

Kayexolate dose

A

15G PO 1-4X daily, can be given rectally

47
Q

Manifestations of hypoK

A

Muscle fatigue, flaccid paralysis, mental confusion, increased urinary output, shallow resps, dysrhytmias

48
Q

HypoK ECG

A

U waves
T wave flattening
ST segment changes
PEA/asystole

49
Q

KCl dose

A

10-20 mEq/hr in non emergent

2 mEq/min for 10 minutes in emerg

50
Q

Causes of hyper Na+

A

Sweating, osmotic diuresis, DI, burns, CNS disorders (thirst) dehydration, diet, hypertonic saline

51
Q

Manifestations of hyperNa

A

Thirst, HTN, edema, agitation, convulsions

52
Q

TX hyperNA

A
Hypotonic fluids (D5W)
Do gradually
53
Q

Total body water =

A

Half of weight in KG

54
Q

Water deficit (L)

A

((Plasma Na+conc-140)/140) X TBW

55
Q

Causes of hypoNa

A
Thiazide diuretics
Renal failure
Vomiting/diarrhea with water intake
Addison
CHF
Cirrhosis
Diet
56
Q

Manifestations of hypoNa

A

Muscle weakness
Dizzy, confusion, stupor coma, headache
Hypotension, tachycardia

57
Q

Tx hypoNa

A

Hypertonic saline (3%) slowly to prevent pontine myelinolysis

58
Q

Na+ deficit =

A

(desired Na+ - current Na+) X 0.6 X bodyweight (kg)

Divide Na deficit by concentration of Na (513 mEq/L) to determine amount delivered

59
Q

Normal mag

A

1.5-2. >2 is hypermag

60
Q

ECG changes in ghyper mag

A
Increased PR/QT intervals
Increased QRS duration
Decreased P wave voltage
Peaked Ts
AV blocks
Asystole
61
Q

Manifestations of hyper mag

A

Hypotension, muscle weakness and paralysis
Decreased reflexes
N/V
Altered LOC

62
Q

TX of hyper mag

A

Calcium as serum levels are controlled by same mechanisms as Mag
Calcium antagonizes effect of mag and K+ at cell membrane
Dialysis, saline and lasix also

63
Q

Calcium dose hyper mag

A

10mL of 10% solution of 10 minutes

64
Q

Hypomag

A
GI loss, malnutrtion
Renal disease
Diuretics, dig, ETOH
Hypothermia
Hypercalcemia
DKA
Thyroid either way
Hypophostate
Burns, sepsis, lactation
65
Q

Hypomag manifestations

A

Weakness, irritability, tetany, paresthesia, delirium, confusion, convulsions, anorexia, N/V, dysrhythmias

66
Q

ECG of hypo mag

A
Prolonged QT/PR intervals
ST depression
T wave inversion
P wave flattening or inversion
Wide QRS
torsades, v-fib
67
Q

TX of hypo mag

A

Mag 2g in 50mL of 10 minutes

CaCl may be used as hypocalcemia is common in hypo mag, or KCl as hypokalemia is common with hypomag

68
Q

Hypercalcemia

A

Normal range is 2.1-2.6 mmol/L

Total 9-10.5 mg/dL

69
Q

Causes of hypercalc

A

Hyperparathyroid
Malignancy
Vit D disorders
Bone disorders

70
Q

Hypercalc ECG

A
Short QT
Long PR/QRS with increases QRS voltage
T wave flattening/widening
QRS notching
AV block
71
Q

Manifestations of hypercalc

A

Lethargy, weakness, anorexia, N/V, polyuria, pruritis, bone pain, depression, confusion stupid coma
Paresthesia

72
Q

TX hypercalcemia

A

IV NS for diuresis
Dialysis for CHF/renal
Agents that reduce bone reabsorption (calcitonon, glucocorticoids)

73
Q

Hypocalcemia

A

Below 2.1mmol/L

74
Q

Hypocalc causes

A
Hypoparathyroid
Hypomag
Hypermag
Vit D deficit
Alkalosis
75
Q

ECG changes hypocalc

A

QT prolongation
T wave inversion
Heart blocks
V fib

76
Q

Manifestations of hypocalc

A
Increased reflexes
Muscle cramps, spasms
Paresthesia
Tetany
Bone fracture
77
Q

TC of hypocalc

A

CaCl 10mL 10% over 10 minutes

Mag, K+ and pH must be treated too

78
Q

Calcium chloride

A

Electrolyte
MOA contraction of muscle via actin myosin
Depol of slow channels via influx during stage 0
regulation of neuronal transmission

79
Q

Pharmacokinetics of CaCl

A

Half bound to albumin
Half ionized (active)
Alkalosis increases albumin binding

80
Q

CaCl uses

A

Hypocalc
Hypermag
HyperK
BB or CCB OD

81
Q

Contras to CaCl

A

Hypercalcemia
Dig tox
Precautions
Dedicated line (preciptate formation) IV only, extravastion will fuck your shit up

82
Q

Dose of CaCl

A

Arrest 1g SIVP Q 10 one time

OD 500mg in 50mL over 10 minutes repeat X1