This document provides an overview of various fluids and electrolytes including potassium, calcium, magnesium, phosphate, creatinine, sodium, and bicarbonate. It discusses the normal ranges, roles, causes of abnormalities, clinical presentations, and treatment approaches for imbalances in each of these electrolytes. Basic concepts covered include renal regulation of electrolytes, shifts between intra- and extracellular fluid, and the importance of fluid balance and sodium for maintaining proper osmolality.

1. +
Fluids and Electrolytes
IM 2013 (AVM)

2. +
Outline
 Potassium
 Calcium
 Magnesium
 Phosphate
 Creatinine and Renal Function
 Water and Sodium
 Bicarbonate
 Inotropes

3. +
Basic Metabolic Panel
Na + Cl- BUN
Ca++
Glu Mg++
K+ CO3
-- Cr Phos--
3

4. +
POTASSIUM

5. +
Potassium (K+)
 Normal range: 3.5-4.5
 Largely contained intra-cellular  SK does not reflect
total body K
 Important roles: contractility of muscle cells,
electrical responsiveness
 Principal regulator: kidneys
5

6. +
Potassium (K+)
 Daily requirement 1-2 mEq/kg
 Complete absorption in the upper GI tract
 Kidneys regulate balance
 10-15% filtered is excreted
 Aldosterone: increase K+ & decrease Na+ excretion
 Mineralocorticoid & glucocorticoid  increase K+ &
decrease Na+ excretion in stool
6

7. +
Potassium (K+)
Acidosis
 Low pH  shifts K+ out of cells (into serum)
 Hi pH  shifts K+ into cells
 0.3-1.3 mEq/L K+ change / 0.1 unit change in pH in
the opposite direction
7

8. +
Hypokalemia
Hypokalemia
 <2.5: life threatening
 Common in severe gastroenteritis
8

9. +
Causes of Hypokalemia
 Distribution from ECF
 Hypokalemic periodic paralysis
 Insulin, Β-agonists,
catecholamines, xanthine
 Decrease intake
 Extra-renal losses
 Diarrhea
 Laxative abuse
 Perspiration
 Excessive colas
consumption
 Renal losses
 DKA
 Diuretics: thiazide, loop
diuretics
 Drugs: amphotericin B,
Cisplastin
 Hypomagnesemia
 Alkalosis
 Hyperaldosteronism
 Licorice ingestion
 Gitelman & Bartter
syndrome
9

10. +
Hypokalemia: Presentation
 Presentation
 Usually asymptomatic
 Skeletal muscle: weakness & cramps; respiratory failure
 Flaccid paralysis & hyporeflexia
 Smooth muscle: constipation, urinary retention
 ECG changes
 Flattened or inverted T-wave
 U wave: prolonged repolarization of the Purkinje fibers
 Depressed ST segment and widen PR interval
 Ventricular fibrillation can happen
10

11. +
Hypokalemia: Presentation
11
Hypokalemia
- Flattened or inverted T-
wave
- U wave: prolonged
repolarization of the Purkinje
fibers
- Depressed ST segment
and widen PR interval
- Ventricular fibrillation can
happen

12. +
Hypokalemia: Treatment
 Address the causes & underlying condition
 Dietary supplements : leafy green vegetables, tomatoes, citrus
fruits, oranges or bananas
 Oral K replacement preferred
 IV: KCl 0.5-1 mEq/kg over 1 hr (rate of 10 mEq/hr)
 K Acetate or K Phos as alternative
 Add K sparing diuretics
 Correct hypomagnesemia
12

13. +
Hypokalemia: Treatment
 30cc Oral KCl = 40mEqs K
 Kalium Durule = 10mEqs K
13

16. +
Causes of Hyperkalemia
Hyperkalemia
 >6.5 – life threatening; Potential lethal arrhythmias
Causes
 Spurious
 Difficult blood draw  hemolysis  false reading
 Increase intake
 Iatrogenic: IV or oral
 Blood transfusions
16

17. +
Causes of Hyperkalemia
 Decrease excretion
 Renal failure
 Adrenal insufficiency or
CAH
 Hypoaldosteronism
 Urinary tract obstruction
 Renal tubular disease
 ACE inhibitors
 Potassium sparing
diuretics
 Trans-cellular shifts
 Acidemia
 Rhadomyolysis; Tumor
lysis syndrome; Tissue
necrosis
 Succinylcholine
 Malignant hyperthermia
17

18. +
Hyperkalemia: Presentation
 Neuromuscular effects
 Delayed repolarization, faster depolarization, slowing of
conduction velocity
 Paresthesias  weakness  flaccid paralysis
 EKG changes
 ~6: peak T waves
 ~7: increased PR interval
 ~8-9: absent P wave with widening QRS complex
 Ventricular fibrillation
 Asystole
18

19. +
Hyperkalemia: Presentation
19

20. +
Hyperkalemia: Treatment
 Lower K+ temporarily
 Calcium gluconate 100mg/kg IV
 Bicarb: 1-2 mEq/kg IV
 Insulin & glucose
 Insulin 0.05 u/kg IV + D10W 2ml/kg then
 Insulin 0.1 u/kg/hr + D10W 2-4 ml/kg/hr
 Salbutamol (β2 selective agonist)
nebulizer
 Increase elimination
 Hemodialysis or hemofiltration
 Kayexalate via feces
 Furosemide via urine
 Calcium: increases threshold
potential  decrease cardiac
cell excitability
 Bicarb: stimulate an exchange
of cellular H+ for Na+, thus stim
Na,K ATPase
 Insulin: shift K into cells via
Na,K-ATPase; last a few hours
 Beta agonist: promote K shift
into cells
20

23. +
CALCIUM

24. +
Calcium
 Normal range: 8.8-10.1 with half bound to albumin
 Ionized (free or active)calcium: 4.4-5.4 – relevant for cell
function
 Majority is stored in bone
 Hypoalbuminemia  falsely decreased calcium
 (alb in g/L): Ca measured + [0.8 x (Albn – Alb m)]
 (alb in g/dL): Ca measured + [(40 – Alb) x 0.02]
24

25. +
Calcium
 Roles:
 Coagulation
 Cellular signals
 Muscle contraction
 Neuromuscular transmission
 Controlled by parathyroid hormone and vitamin D
25

27. +
Hypocalcemia: Presentation
 Neuromuscular irritability
 Paresthesias: oral, perioral and acral, tingling or pin & needles
 Tetany (Chvostek & Trousseau signs)
 Hyperreflexia
 Laryngospasm
 Jittery, poor feedings or vomiting in newborns
 ECG changes: prolonged QT intervals
27

28. +
Hypocalcemia: Treatment
 Supplements
 IV: gluconate or chloride with EKG change
 Oral calcium with vitamin D
 Calcium gluconate 10ml 10% wt/vol (90mg or 2.2mmol) IV,
diluted in 50ml of 5%dextrose or 0.9%NaCl
 Infusion: 10amps Ca gluc or 900mg Ca in 1L of D5 or
0.9%NaCl over 24hrs
 Treat accompanying hypomagnesemia
28

30. +
Hypercalcemia: Presentation
 Groans: constipation
 Moans: psychic moans (fatigue, lethargy, depression)
 Bones: bone pain
 Stones: kidney stones
 Psychiatric overtones: depression & confusion
 Fatigue, anorexia, nausea, vomiting, pancreatitis
 ECG: short QT interval, widened T wave
30

31. +
Hypercalcemia: Treatment
 Fluid & diuretics
 4-6L of IV saline may be needed in first 24hrs
 Forced diuresis with loop diuretic
 Oral supplement: biphosphate or calcitonine
 Zoledronic acid (4mg IV over 30mins)
 Pamidronate (60-90 IV over 2-4hrs)
 Etidronate (7.5mg/kg/d for 3-7d)
 Onset 1-3days
 Glucocorticoids
 IV hydrocortisone 100-300mg daily
 Oral prednisone (40-60mg daily for 3-7d)
 Dialysis
31

32. +
MAGNESIUM

33. +
Magnesium
 Normal range: 1.5-2.3
 60% stored in bone
 1% in extracellular space
 Necessary cofactor for many enzymes
 Renal excretion is primary regulation
33

36. +
Hypomagnesemia: Presentation
 Weakness, muscle cramps
 Cardiac arrhythmias
 Prolonged PR, QRS & QT
 Torsade de pointes
 Complete heart block & cardiac arrest with level >15
 CNS: irritability, tremor, athetosis, jerking,
nystagmus
 Hallucination, depression, epileptic fits, HTN,
tachycardia, tetany
36

37. +
Hypomagnesemia: Treatment
 Oral or IV supplement
 Oral MgCl2, MgO, Mg(OH)2: in divided doses totalling
20-30mmol/d (40-60meq/d)
 IV MgCl2 as infusion of 50mmol/d (100meq/d)
 May also give MgSO4 IV
 Correct ongoing loss
 Correct for calcium, potassium, and phosphate as
well
37

39. +
Hypermagnesemia Presentation
 Weakness, nausea, vomiting
 Hypotension, hypocalcemia
 Arrhythmia and asystole
 4.0 mEq/L hyporeflexia
 >5 prolonged AV conduction
 >10 complete heart block
 >13 cardiac arrest
39

40. +
Hypermagnesemia: Treatment
 Magnesium-free cathartics or enemas
 IV hydration
 Calcium infusion
 IV in doses of 100-200 over 1-2hrs
 Diuretics
 Dialysis
40

41. +
PHOSPHORUS

42. +
Phosphorus
 Normal range: 2.3 - 4.8
 Most store in bone or intracellular space
 <1% in plasma
 Intracellular major anion, most in ATP
 Concentration varies with age, higher during early childhood
 Necessary for cellular energy metabolism
42

46. +
Hypophosphotemia
 Presentation:
 Muscle dysfunction and weakness: diploplia, low CO,
dysphagia, respiratory depression
 AMS
 WBC dysfunction
 Instability of cell membrane  rhabdomyolysis
 Treatments
 Supplementation with IV as neutral mixtures of Na and
Phos salts
 Oral phosphate 750-2000mg in divided doses
 Necessary to avoid Ca-Phos product >50
 Correct hypocalcemia
46

47. +
Hyperphosphotemia
Presentation:
 Tetany, seizures, accelerated nephrocalcinosis,
pulmonary and cardiac calcifications (mainly due to
widespread calcium phosphate precipitates)
Treatments
 Limited
 Volume expansion
 Aluminum hydroxide antacids or sevelamer for
chelating
 Hemodialysis
47

48. +
Creatinine and Renal
Function

49. +
BUN/CREA RATIO
BUN / Crea x 247
 > 20:1 prerenal azotemia
 10-15:1 oliguric acute renal failure

50. +
Creatinine Clearance Estimation
(Cockcroft-Gault)
 Female = Male x 0.85
 (lower fraction of body weight is muscle the metabolism of which yields
creatinine)

52. +
CKD
Stage
Description GFR
mL/min/1.73
m2
1 Kidney damage w/ normal /
increased
90
2 GFRKidney damage w/
mildly decreased
60-89
3 GFRModerately decreased
GFR
30-59
4 Severely decreased GFR 15-29
5 Renal failure < 15 (or
dialysis)

53. +
WATER and SODIUM

54. +
Sodium (Na+)
 Bulk cation of extracellular fluid  change in SNa
reflects change in total body Na+
 Principle active solute for the maintenance of
intravascular & interstitial volume
 Absorption: throughout the GI system via active
Na,K-ATPase system
 Excretion: urine, sweat & feces
 Kidneys are the principal regulator
54

55. +
Sodium (Na+)
 Kidneys are the principal regulator
 2/3 of filtered Na+ is reabsorbed by the proximal convoluted
tubule, increase with contraction of extracellular fluid
 Countercurrent system at the Loop of Henle is responsible for
Na+ (descending) & water (ascending) balance – active
transport with Cl-
 Aldosterone stimulates further Na+ re-absorption at the distal
convoluted tubules & the collecting ducts
 <1% of filtered Na+ is normally excreted but can vary up to
10% if necessary
55

56. +
Sodium (Na+)
Normal SNa: 135-145
Major component of serum osmolality
 Sosm = (2 x Na+) + (BUN / 2.8) + (Glu / 18)
 Normal: 285-295
Alterations in SNa reflect an abnormal water
regulation
56

57. +
Sodium (Na+)
Hyponatremia
 Na+<135
 Seizure threshold ~125
 <120 life threatening
57

59. +
Hyponatremia: Presentation
 Cellular swelling due to water shifts into cells
 Anorexia, nausea, emesis, malaise, lethargy,
confusion, agitation, headache, seizures, coma
 Chronic hyponatremia: better tolerated
59

60. +
Hyponatremia: Treatment
 Rapid correction  central pontine myelinolysis
 Goal 12 mEq/L/day
 Fluid restriction with SIADH
 Hyponatremic seizures
 Poorly responsive to anti-convulsants
 Hypertonic saline
 Need to bring Na to above seizure threshold
60

62. +
Causes of Hypernatremia
 Excessive intake
 Improperly mixed formula
 Exogenous: bicarb, hypertonic saline, seawater
Water deficit:
 Central & nephrogenic DI
 Increased insensible loss
 Inadequate intake
62

63. +
Causes of Hypernatremia
 Water and sodium deficit
 GI losses
 Cutaneous losses
 Renal losses
 Osmotic diuresis: mannitol, diabetes mellitus
 Chronic kidney disease
 Polyuric ATN
 Post-obstructive diuresis
63

64. +
Hypernatremia: Presentation
 Dehydration
 “Doughy” feel to skin
 Irritability, lethargy, weakness
 Intracranial hemorrhage
 Thrombosis: renal vein, dura sinus
64

65. +
Hypernatremia: Treatment
 Rate of correction for Na+ 1-2 mEq/L/hr
 Calculate water deficit
 Water deficit = 0.6 x wt (kg) x [(current Na+/140) – 1]
 Rate of correction for calculated water deficit
 50% first 12-24 hrs
 Remaining next 24 hrs
65

67. +
Sodium (Na+)
Urine
Output
Serum
Na
Urine
Na
Serum
Osm
Urine
Osm
DI
SIADH
CSW

68. +
Serum or Plasma Osmolality
2Na + Glu + BUN
 Normal 280-290 mosmol/kg
 Use in plasma osmolal gap

69. +
Urine Osmolality (mosmol/kg)
2 (urine Na + urine K) +
urine urea + urine
glucose
 Use in urine osmolal gap

70. +
Water Deficit
 = [(Plasma Na – 140) / 140] x total body water in hypernatremia due to
water loss
 [(Plasma Na – 140) / 140] x
[(0.5 in men or 0.4 in women)
x lean body weight]
 Use in hypernatremia due to water loss, but should
be corrected slowly over at least 48-72h, ideally w/
hourly serum Na determination to target 0.5
mmol/L/h but not > 12 mmol/L over the 1st 24h.

71. +
Ideal Body Weight
 For men = (106 lb for the first 5 ft + 6 lb for each inch
above 5 ft) / 2.2 lb/kg
 For women = (100 lb for the first 5 ft + 5 lb for each
additional inch) / 2.2 lb/kg

72. +
24-hr Urine Collection Adequacy
 Creatinine is produced at a constant rate & in an
amount directly proportional to skeletal muscle mass
 Creatinine coefficient = 23 mg/kg of ideal body
weight in men & 18 mg/kg of IBW in women
 If 24 h urine creatinine < IBW x creatinine coefficient
 inadequately collected specimen
 Unpredictable when serum crea > 530 umol/L

75. +
FLUIDS

76. +
Crystalloids
SOLUTIONS pH Osm Kcal Na K Cl Ca Mg Lactate Acetate
(A) ISOTONIC
1. PNSS 5.7 308 - 15
4
- 15
4
- - - -
2. D5NSS 4.2 560 200 15
4
- 15
4
- - - -
3.D5NR 5.4 552 200 14
0
5 98 - 3 - 27
4. D5 Eurosol-R 4.6-6.5 552 200 14
0
5 98 - 3 - 50
5. D5LR 5.3 527 200 13
0
4 10
9
3 - 28 -
6. D5 Euromed LR 3.5-6.5 525 200 13
0
4 10
9
2.
7
- 28 -
7.D5 LVP LR 3.5-5.0 586 200 14
7
4 15
8
2.
2
- 28 -
8.Plasmasol 148 4-6 547 200 14
0
5 98 - 3 - 27

77. +
SOLUTIONS pH Osm Kcal Na K Cl Ca Mg Lactate Acetate
(B) HYPOTONIC
1.D5NM 5.2 368 200 40 1
3
40 - 3 - 16
2. D5 Eurosol 4.5-6.5 368 200 40 1
3
40 - 3 - 16
3.D5 Ionosol MB 4.7 350 200 25 2
0
22 - 3 23 -
4.D5 Eurolon 4.6-6.5 350 200 25 2
0
22 - 3 23 -
5. Plasmasol 48 4-6 348 200 25 2
0
24 - 3 23 -
6. D50 .45
Euromed
3.5-6.5 408 200 77 - 77 - - - -

78. +
BICARBONATE

79. +
Bicarbonate
 Normal range: 25-35
 Important buffer system in acid-base homeostasis
 Increased in metabolic alkalosis or compensated
respiratory acidosis
 Decreased in metabolic acidosis or compensated
respiratory alkalosis
 0.15 pH change/10 change in bicarb in
uncompensated conditions
79

80. +
Indications for HCO3 Therapy
 pH < 7.2 and HCO3 < 5 – 10 mmHg
 When there is inadequate ventilatory compensation
 Elderly on beta blockers in severe acidosis with compromised
cardiac function
 Concurrent severe AG and NAGMA
 Severe acidosis with renal failure or intoxication

81. +
Complications of HCO3 Therapy
 Volume overload
 Hypernatremia
 Hyperosmolarity
 Hypokalemia
 Intracellular acidosis
 Causes overshoot alkalosis
 Stimulates organic acid production
  tissue O2 delivery
NaHCO3 50 ml = 45 mEq Na
NaHCO3 gr X tab = 7 mEq Na

82. +
Bicarbonate Deficit
 = HCO3 space x (desired HCO3 – measured HCO3)
(0.5-0.8* x body weight in kg) x
(24** – measured HCO3)
 * increases w/ increasing severity of the acidosis,
normally 50% of body weight but increases to 80%
in severe acidosis as a reflection of the total body
buffering capacity.
 ** For severe acidosis < pH 7.20 in pure HAGMA,
goal is to increase HCO3 to 10 mEq/L & pH to 7.15.

83. +
 Goal is to increase plasma HCO3 slowly to 20-22 mEq/L.
Notice that the formula uses 24 as the normal bicarbonate.
 It tells us what the deficit is, but not what we should give the
patient.
 We still follow the targets for the above conditions (i.e., use
them instead of 24). HCO3 therapy does not come without
complications.

84. +
SHOCK and INOTROPES

86. +
Dobutamine (ugtts/min)
desired dose x body weight
in kg / (16.6 * strength)
 Desired dose 2-20 mcg/kg/min
 For dobutamine 250 mg/amp 1 amp in 250 mL D5W, strength is
1 (if 2 amps for CHF, 2 and so on)

87. +
Dopamine (ugtts/min)
desired dose x body weight
in kg / (13.3 * strength)
 Desired dose 5-15 mcg/kg/min
 For dopamine 200 mg/amp 1 amp in 250 mL D5W, strength is 1
(if 2 amps for CHF, 2 and so on)

88. +
Norepinephrine (ugtts/min)
desired dose x body weight
in kg / (0.133 * strength)
 Desired dose 0.5-30 mcg/kg/min
 For norepinephrine 2 mg/amp 1 amp in 250 mL D5W, strength
is 1 (if 2 amps for CHF, 2 and so on)

89. +
END.