Fluid & Electrolyte Disorders.

1. DR. PADMAJA PALLAVI PANDEY

2. INTRODUCTION:
FLUIDS & ELECTROLYTE
DISORDERS
 Objectives
 Fluid Balance
 Solute Homeostasis
 Regulation of Body Water
 Volume Abnormalities
 Fluid Volume Deficit
 Fluid Volume Excess

3. CONT.
 Basic Metabolic Panel
 Electrolytes
 Sodium - Hyponatremia & Hypernatremia
 Potassium - Hypokalemia & Hyperkalemia
 Calcium – Hypocalcemia & Hypercalcemia
 Magnesium – Hypomagnesemia & Hypermagnesemia

4. OBJECTIVES
 Recognize common fluid and electrolyte disorders
 Clinical presentations
 Management

5. 5
Total body water (TBW)

6. 6
 Fluid compartments are separated by membranes that
are freely permeable to water – but impermeable to
solutes.
 Movement of fluids is due to:
 hydrostatic pressure differentials
 osmotic pressure differentials

7. 7
Fluid Balance

8. 8
Fluid Balance(Cont’d)
The body tries to maintain homeostasis of fluids and
electrolytes by regulating:
 Volumes
 Solute charge and osmotic load

9. 9
Solute Homeostasis
 Electrolytes – charged particles
 Cations – positively charged ions
 Na+, K+ , Ca++, H+
 Anions – negatively charged ions
 Cl-, HCO3
- , PO4
3-
 Non-electrolytes - Uncharged particles
 Proteins, urea, glucose, O2, CO2

10. 10
Maintained by:
 Ion transport
 Water movement
 Kidney function
These functions act to keep body fluids:
 Electrically neutral
 Osmotically stable (specified number of particles
per volume of fluid)
Solute Homeostasis

11. 11
Where sodium goes, water follows.
Diffusion – movement of particles down a
concentration gradient.
Osmosis – diffusion of water across a selectively
permeable membrane
Active transport – movement of particles up a
concentration gradient; requires energy
Solute Homeostasis

12. 12

13. 13
Regulation of body water
The default is get rid of it
The control processes include:
Release of ADH (antidiuretic hormone)
Thirst

14. Regulation of body water
Any of the following:
• Decreased amount of water in body
• Increased amount of Na+ in the body
• Increased blood osmolality
• Decreased circulating blood volume
Results in:
• Stimulation of osmoreceptors in hypothalamus
• Release of ADH from the posterior pituitary
• Increased thirst
And thus: water consumption and conservation

15. 15
Volume Abnormalities
Isotonic fluid loss
 ↓ECF volume, weight loss, dry skin and mucous
membranes, ↓ urine output: hypovolemic shock

16. 16
Volume Abnormalities
Isotonic fluid gain
 ↑ECF volume, weight gain, decreased hematocrit,
diluted plasma proteins, distended neck veins, ↑
B.P:
anasarca

17. 17
Volume Abnormalities
Edema
the accumulation of fluid within the interstitial space
Causes:
• increased hydrostatic pressure
• venous obstruction, lymphedema, CHF, renal failure
• lowered plasma osmotic pressure (protein loss)
• liver failure, malnutrition, burns
• increased capillary membrane permeability
• Inflammation, SIRS, sepsis

18. 18
Volume Abnormalities
Edema
the accumulation of fluid within the interstitial space.
Results in:
• increased distance for diffusion
• impaired blood flow
• slower healing
• increased risk of infection
• pressure sores over bony prominences
• impaired organ function (brain, liver, gut, kidney)

19. Fluid Volume Deficit
(Hypovolemia, Isotonic Dehydration)
 Common Causes
 Hemorrhage
 Vomiting
 Diarrhea
 Burns
 Diuretic therapy
 Fever
 Impaired thirst

20. Clinical Manifestations
 Signs/Symptoms
 Weight loss
 Thirst
 Orthostatic changes in pulse rate and BP
 Weak, rapid pulse
 Decreased urine output
 Dry mucous membranes
 Poor skin turgor

21. Treatment/Interventions (FVD)
 Fluid Management
 Diet therapy – Mild to moderate dehydration.
Correct with oral fluid replacement.
 Oral rehydration therapy – Solutions containing
glucose and electrolytes. E.g., Pedialyte,
Rehydralyte.
 IV therapy – Type of fluid , ordered depends on the
type of dehydration and the patient’s cardiovascular
status.

22. Fluid Volume Excess
 Common Causes:
 Congestive Heart Failure
 Early renal failure
 IV therapy
 Excessive sodium ingestion
 SIADH
 Corticosteroid

23. Clinical Manifestations
 Signs/Symptoms
 Increased BP
 Bounding pulse
 Venous distention
 Pulmonary edema
 Dyspnea
 Orthopnea (difficulty in breathing , when supine)
 Crackles

24. Treatment/Interventions (FVE)
 Drug therapy
 Diuretics may be ordered if renal failure is not the
cause.
 Restriction of sodium and saline intake
 I/O
 Weight

25. Basic Metabolic Panel
Na + Cl- BUN Ca++
Glu Mg++
K+ CO3
-- Cr Phos--
25

26. 26
Electrolytes

27. Basic Metabolic Panel
Na + Cl- BUN Ca++
Glu Mg++
K+ CO3
-- Cr Phos--
27

28. 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

29. CONT.
 Kidneys are the principal regulator
 2/3 of filtered Na+ is reabsorbed by the proximal
convoluted tubule, increase with contraction of
extracellular fluid
 <1% of filtered Na+ is normally excreted but can vary
up to 10% if necessary.

30. CONT.
 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.

31. CONT.
 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

32. HYPONATREMIA (<135mEq/L)
SYMPTOMS :-
 Anorexia
 Headache
 Nausea
 Emesis
 Impaired response to verbal stimuli
 Impaired response to painful stimuli
 Bizarre behavior
 Hallucinations
 Obtundation
 Incontinence
 Respiratory insufficiency
 Decorticate or decerebrate posturing

33. CONT.
 Bradycardia
 Hypertension or hypotension
 Altered temperature regulation
 Dilated pupils
 Seizure activity
 Respiratory arrest
 Coma
 Hypotension
 Renal failure as consequence of hypotension
 Tachycardia
 Weakness
 Muscular cramps

34. CONT.
EVALUATION :-
 Volume
 Serum sodium, osmolality, BUN/Creatinine
 Urine sodium, osmolality

35. CONT.
 1) Hypovolemic hyponatremia
 Renal losses caused by diuretic excess, osmotic
diuresis , salt-wasting nephropathy, adrenal
insufficiency, proximal renal tubular acidosis,
metabolic alkalosis, and pseudohypoaldosteronism
result in a urine sodium concentration greater than
20 mEq/L
 Extrarenal losses caused by vomiting, diarrhea,
sweat, and third spacing result in a urine sodium
concentration less than 20 mEq/L
 Rx: Volume resuscitation with NS.

36. CONT.
 2) Normovolemic hyponatremia
 When hyponatremia is caused by SIADH, reset
osmostat, glucocorticoid deficiency, hypothyroidism,
or water intoxication, urine sodium concentration is
greater than 20 mEq/L
 Rx:
 Fluid restriction
 Correct endocrine abnormality

37. CONT.
 3) Hypervolemic hyponatremia
 If hyponatremia is caused by an edema-forming state
(eg, congestive heart failure, cirrhosis, nephrotic
syndrome), urine sodium concentration is less than
20 mEq/L
 If hyponatremia is caused by acute or chronic renal
failure, urine sodium concentration is greater than 40
mEq/L
 Rx: Correct underlying state

38. CONT.
Contributing Factors :-
 Excessive diaphoresis
 Wound Drainage
 NPO
 CHF
 Low salt diet
 Renal Disease
 Diuretics

39. CONT.
Assessment findings:-
 Neuro - Generalized skeletal muscle weakness.
Headache / personality changes.
 Resp.- Shallow respirations
 CV - Cardiac changes depend on fluid volume
 GI – Increased GI motility, Nausea, Diarrhea
(explosive)
 GU - Increased urine output

40. CONT.
Interventions/Treatment :-
 Restore Na levels to normal and prevent further
decreases in Na.
 Drug Therapy –
 (FVD) - IV therapy to restore both fluid and Na.
If severe may see 2-3% saline.
 (FVE) – Administer osmotic diuretic (Mannitol)
to excrete the water rather than the sodium.
 Increase oral sodium intake and restrict oral fluid
intake.

41. CONT.
 Correct serum Na by 1mEq/L/hr
 Check serum Na q4hr
 Use 3% saline in severe hyponatremia
 Goal is serum Na 130
 Avoid too rapid correction:
 Central pontine myelinolysis
 Flash pulmonary edema

42. 42
Acute Hyponatremia
 Na < 120 and duration < 48 hrs
 Etiology:
 Postoperative
 Exercise with hypotonic fluid replacement
 Drugs - Ecstasy
 Treat aggressively using 3% saline to raise Na by
5mm/L in one hour
 Beware rapid drop in vasopressin levels

43. HYPERNATREMIA(>145mEq/L)
 Plasma Na+ > 145 mEq / L
 Due to ↑ Na + or ↓ water
 Water moves from ICF → ECF
 Cells dehydrate

44. CONT.
Due to:
 Excess Na intake (hypertonic IV solution)
 Excess Na retention (oversecretion of aldosterone)
 Loss of pure water
 Long term sweating with chronic fever
 Respiratory infection → water vapor loss
 Diabetes (mellitus or insipidus) – polyuria
 Insufficient intake of water (hypodipsia)

45. CONT.
Contributing Factors :-
 Hyperaldosteronism
 Renal failure
 Corticosteroids
 Increase in oral Na intake
 Na containing IV fluids
 Decreased urine output with increased urine
concentration.

46. CONT.
Contributing Factors(Cont’d) :-
 Diarrhea
 Dehydration
 Fever
 Hyperventilation

47. CONT.
Assessment findings:-
 Neuro - Spontaneous muscle twitches . Irregular
contractions. Skeletal muscle weakness .
Diminished deep tendon reflexes
 Resp. – Pulmonary edema
 CV – Diminished CO. HR and BP depend on
vascular volume.
 GU – Dec. urine output. Inc. specific gravity.
 Skin – Dry, flaky skin. Edema related to fluid volume
changes.

48. CONT.
Evaluation :-
 Volume
 Serum sodium, osmolality, BUN/Creatinine
 Urine sodium, osmolality.

50. CONT.
Interventions/Treatment :-
 Drug therapy
 (FVD) .45% NS. If caused by both Na and fluid
loss, will administer NaCL . If inadequate , renal
excretion of sodium, will administer diuretics.
 Diet therapy
 Mild – Ensure water intake

51. CONT.
 Calculate the free water deficit:
 0.6 x wt (kg) x (patient’s sodium/140 - 1)
 Correct the free water deficit at a rate of 1mEq/L/hr
 Check serum Na q4hr
 Use isotonic salt-free IV fluid

52. Basic Metabolic Panel
Na + Cl- BUN Ca++
Glu Mg++
K+ CO3
-- Cr Phos--
52

53. Potassium (K+)
 Normal range: 3.5-5.0
 Largely contained intra-cellular  SK does not reflect
total body K
 Important roles: contractility of muscle cells, electrical
responsiveness
 Principal regulator: kidneys

54. CONT.
 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

55. CONT.
 Solvent drug
 Increase in Sosmo  water moves out of cells  K+
follows.
 Increase 0.6 SK /Increase 10 of Sosmo
 Evidence of solvent drug in diabetic ketoacidosis
 Acidosis
 Low pH  shifts K+ out of cells (into serum)
 High pH  shifts K+ into cells
 0.3-1.3 mEq/L K+ change / 0.1 unit change in pH in
the opposite direction

56. HYPOKALEMIA (<3.5mEq/L)
 Serum K+ < 3.5 mEq /L
 Beware if diabetic
 Insulin pushes K+ into cells
 Ketoacidosis – H+ replaces K+, which is lost in urine
 β – adrenergic drugs or epinephrine
Pathophysiology :-
Decrease in K+ causes decreased excitability of cells,
therefore cells are less responsive to normal stimuli.

57. CONT.
Contributing Factors :-
 Diuretics
 Shift into cells
 Digitalis
 Water intoxication
 Corticosteroids
 Diarrhea
 Vomiting

58. CONT.
CAUSES :-
 Decreased intake of K+
 Increased K+ loss
 Chronic diuretics
 Severe vomiting/diarrhea
 Acid/base imbalance
 Trauma and stress
 Increased aldosterone
 Redistribution between ICF and ECF

60. CONT.
Interventions/Treatment :-
 Assess and identify those at risk
 Encourage potassium-rich foods
 K+ replacement (IV or PO)
 Monitor lab values
 D/c potassium-wasting diuretics
 Treat underlying cause.

61. HYPERKALEMIA (>5.0mEq/L)
 Serum K+ > 5.5 mEq / L
 Check for renal disease
 Massive cellular trauma
 Insulin deficiency
 Addison’s disease
 Potassium sparing diuretics
 Decreased blood pH
 Exercise pushes K+ out of cells
Pathophysiology :-
An inc. in K+ causes increased excitability of cells.

62. CONT.
Contributing Factors :-
 Increase in K+ intake
 Renal failure
 K+ sparing diuretics
 Shift of K+ out of the cells

64. CONT.
Interventions/Treatment :-
 Need to restore normal K+ balance:
 Eliminate K+ administration
 Inc. K+ excretion
 Lasix
 Kayexalate (Polystyrene sulfonate)
 Cardiac Monitoring

65. CONT.
 10% Calcium Gluconate or Calcium Chloride
 Insulin (0.1U/kg/hr) and IV Glucose
 Metabolic alkalosis (if the patient is acidemic)
 1 L H20 with 150meq of NaHCO3
 Hemodialysis

66. Basic Metabolic Panel
Na + Cl- BUN Ca++
Glu Mg++
K+ CO3
-- Cr Phos--
66

67. 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
 Cac = Cam + [0.8 x (Albn – Alb m)]

68. CONT.
 Roles:
 Coagulation
 Cellular signals
 Muscle contraction
 Neuromuscular transmission
 Controlled by parathyroid hormone and vitamin D

69. HYPOCALCEMIA (<9.0mg/dL)
Contributing Factors :-
 Dec. oral intake
 Lactose intolerance
 Dec. Vitamin D intake
 End stage renal disease
 Diarrhea

70. CONT.
Contributing Factors(Cont’d) :-
 Acute pancreatitis
 Hyperphosphatemia
 Immobility
 Removal or destruction of parathyroid gland

71. CONT.
Assessment findings :-
 Neuro –Irritable muscle twitches.
 Positive Trousseau’s sign.
 Positive Chvostek’s sign.
 Resp. – Resp. failure d/t muscle tetany.
 CV – Dec. HR., dec. BP, diminished
peripheral pulses
 GI – Inc. motility. Inc.BS. Diarrhea

72. Positive Trousseau’s Sign

73. Positive Chvostek’s Sign

74. CONT.
Interventions/Treatment :-
 Drug Therapy
 Calcium supplements
 Vitamin D
 Diet Therapy
 High calcium diet
 Prevention of Injury
 Seizure precautions

75. HYPERCALCEMIA (>10.5mg/dl)
Contributing Factors :-
 Excessive calcium intake
 Excessive vitamin D intake
 Renal failure
 Hyperparathyroidism
 Malignancy
 Hyperthyroidism

76. CONT.
Assessment findings :-
 Neuro – Disorientation, lethargy, coma, profound
muscle weakness
 Resp. – Ineffective resp. movement
 CV - Inc. HR, Inc. BP. , Bounding peripheral pulses,
Positive Homan’s sign.
Late Phase – Bradycardia, Cardiac arrest
 GI – Dec. motility. Dec. BS. Constipation
 GU – Inc. urine output. Formation of renal calculi

77. CONT.
Interventions/Treatment :-
 Eliminate calcium administration
 Drug Therapy
 Isotonic NaCL (Inc. the excretion of Ca)
 Diuretics
 Calcium reabsorption inhibitors (Phosphorus)
 Cardiac Monitoring

78. Basic Metabolic Panel
Na + Cl- BUN Ca++
Glu Mg++
K+ CO3
-- Cr Phos--
78

79. 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

80. HYPOMAGNESEMIA (<1.4mEq/L)
Contributing Factors :-
 Malnutrition
 Starvation
 Diuretics
 Aminoglcoside antibiotics
 Hyperglycemia
 Insulin administration

81. CONT.
Assessment findings :-
*Neuro - Positive Trousseau’s sign. Positive Chvostek’s
sign. Hyperreflexia. Seizures
*CV – ECG changes. Dysrhythmias. HTN
*Resp. – Shallow resp.
*GI – Dec. motility, Anorexia, Nausea

82. CONT.
Interventions/Treatment :-
 Eliminate contributing drugs
 IV MgSO4
 Assess DTR’s hourly with MgSO4
 Diet Therapy

83. HYPERMAGNESEMIA
(>2.0mEq/L)
Contributing Factors :-
 Increased Mag intake
 Decreased renal excretion

84. CONT.
Assessment findings :-
 Neuro – Reduced or weak DTR’s. Weak voluntary
muscle contractions. Drowsy to the point of lethargy.
 CV – Bradycardia, peripheral vasodilatation,
hypotension. ECG changes.

85. CONT.
Interventions/Treatment :-
 Eliminate contributing drugs
 Administer diuretic
 Calcium gluconate reverses cardiac effects
 Diet restrictions

86. THANK YOU