electrolytes. Imbalance management......

Sodium (Na)

Bulk cation of extracellular fluid → change in S reflects change in total body Na

Principle active solute for the maintenance of intravascular & interstitial volume

Absorption: throughout the Gl system via active Na, K-ATPase system

Excretion: urine, sweat & feces

Kidneys are the principal regulator

Intracellular Na is constant and important in cellular

activity

Balance btw intake & excretion. Poorly understood mechanism. Some salt craving in some salt wasting

diseases

High sodium concentration in cow's milk.

Children take in less

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
Sodium (Na)

Normal S Na: 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

Sodium (Na)

Hypernatremia:

Causes

Excessive intake

Improperly mixed formula

Exogenous: bicarb, hypertonic saline, seawater

Water deficit:

Central & nephrogenic DI

Increased insensible loss

Inadequate intake.................
Sodium (Na)

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

16

17

Central pontine myelinolysis - rapid correction of hyponatremia water shifts from cell to extracellular space; sx; quadraparesis, dysphagia, dysarthria, diploplia, LOC associated with brain stem damage; no tx; poor prognosis; most die; survival 1/3; 1/3; 1/3 (recovered, disabled and severely disabled)

Sz threshold 125;

HS: 5cc/kg 3-4 mEq/L

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

35

Potassium (K)

Daily requirement 1-2 mEq/kg

Complete absorption in the upper Gl tract

Kidneys regulate balance

10-15% filtered is excreted

Aldosterone: increase K & decrease Na excretion

Mineralocorticoid & glucocorticoid → increase K & decrease Na excretion in stool

- Major secretion again active Na re-absorption; also associated with H+ and NH3 excretion
Potassium (K)

Hypokalemia

Causes

Renal losses

DKA

Diuretics: thiazide, loop diuretics

Drugs: amphotericin B, Cisplastin

Hypomagnesemia

Alkalosis

Hyperaldosteronism

Licorice ingestion

Gitelman & Bartter syndrome

49

DKA: urine loss due to polyuria & volume contracion, also as cationic partner to the negatively charge ketone, Bet

1. Electrolytes Imbalances BM DESDERIUS ( MD, MMED, FCP, MPH ) LECTURER DEPT. INT MED CUHAS

2. Objectives Recognize common fluid and electrolyte disorders Clinical presentations Management

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

4. Basic Metabolic Panel Na + Cl - BUN Ca ++ Glu Mg ++ K + CO 3 -- Cr Phos -- 4

5. Basic Metabolic Panel Na + Cl - BUN Ca ++ Glu Mg ++ K + CO 3 -- Cr Phos -- 5

6. Sodium (Na + ) Bulk cation of extracellular fluid  change in S Na 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 6

7. 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 7

8. Sodium (Na + ) Normal S Na : 135-145 Major component of serum osmolality S osm = (2 x Na + ) + (BUN / 2.8) + (Glu / 18) Normal: 285-295 Alterations in S Na reflect an abnormal water regulation 8

9. Sodium (Na + ) Hypernatremia: Causes Excessive intake Improperly mixed formula Exogenous: bicarb, hypertonic saline, seawater Water deficit: Central & nephrogenic DI Increased insensible loss Inadequate intake 9

10. Sodium (Na + ) Hypernatremia: Causes Water and sodium deficit GI losses Cutaneous losses Renal losses Osmotic diuresis: mannitol, diabetes mellitus Chronic kidney disease Polyuric ATN Post-obstructive diuresis 10

11. Sodium (Na + ) Hypernatremia Clinical presentation Dehydration “Doughy” feel to skin Irritability, lethargy, weakness Intracranial hemorrhage Thrombosis: renal vein, dura sinus 11

12. Sodium (Na + ) 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 12

13. Sodium (Na + ) Hyponatremia Na + <135 Seizure threshold ~125 <120 life threatening 13

14. Sodium (Na + ) Hyponatremia: Etiology Hypervolemic CHF Cirrhosis Nephrotic syndrome Hypoalbuminemia Septic capillary leak Hypovolemic Renal losses Cerebral salt wasting Extra-renal losses aldosterone effect GI losses Third spacing 14

15. Sodium (Na + ) Hyponatremia: Etiology Euvolemic hyponatremia SIADH Glucocorticoid deficiency Hypothyroidism Water intoxication Psychogenic polydipsia Diluted formula Beer potomania Pseudo-hyponatremia Hyperglycemia S Na decreased by 1.6/100 glucose over 100 15 -

16. Sodium (Na + ) Hyponatremia Clinical presentation Cellular swelling due to water shifts into cells Anorexia, nausea, emesis, malaise, lethargy, confusion, agitation, headache, seizures, coma Chronic hyponatremia: better tolerated 16

17. Sodium (Na + ) 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 17

18. Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

19. Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

20. Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

21. Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

22. Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

23. Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

24. Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

25. Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

26. Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

27. Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

28. Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

29. Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

30. Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

31. Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

32. Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

33. Sodium (Na + ) Fill in the blanks Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

34. Basic Metabolic Panel Na + Cl - BUN Ca ++ Glu Mg ++ K + CO 3 -- Cr Phos -- 34

35. Potassium (K + ) Normal range: 3.5-4.5 Largely contained intra-cellular  S K does not reflect total body K Important roles: contractility of muscle cells, electrical responsiveness Principal regulator: kidneys 35

36. 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 36

37. Potassium (K + ) Solvent drag Increase in S osmo  water moves out of cells  K + follows 0.6 S K / 10 of S osmo Evidence of solvent drag in diabetic ketoacidosis 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 37

38. Potassium (K + ) Hyperkalemia >6.5 – life threatening Potential lethal arrhythmias 38

39. Potassium (K + ) Hyperkalemia Causes Spurious Difficult blood draw  hemolysis  false reading Increase intake Iatrogenic: IV or oral Blood transfusions 39

40. Potassium (K + ) Hyperkalemia Causes Decrease excretion Renal failure Adrenal insufficiency or CAH Hypoaldosteronism Urinary tract obstruction Renal tubular disease ACE inhibitors Potassium sparing diuretics 40

41. Potassium (K + ) Hyperkalemia Causes Trans-cellular shifts Acidemia Rhadomyolysis; Tumor lysis syndrome; Tissue necrosis Succinylcholine Malignant hyperthermia 41

42. Potassium (K + ) Hyperkalemia Clinical presentation Neuromuscular effects Delayed repolarization, faster depolarization, slowing of conduction velocity Paresthesias  weakness  flaccid paralysis 42

43. Potassium (K + ) Hyperkalemia Clinical presentation EKG changes ~6: peak T waves ~7: increased PR interval ~8-9: absent P wave with widening QRS complex Ventricular fibrillation Asystole 43

44. Potassium (K + ) 44

45. Potassium (K + ) 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 ( β 2 selective agonist) nebulizer 45

46. Potassium (K + ) Hyperkalemia Treatment Increase elimination Hemodialysis or hemofiltration Kayexalate via feces Furosemide via urine 46

47. Potassium (K + ) Hypokalemia <2.5: life threatening Common in severe gastroenteritis 47

48. Potassium (K + ) Hypokalemia Causes Distribution from ECF Hypokalemic periodic paralysis Insulin, Β -agonists, catecholamines, xanthine Decrease intake Extra-renal losses Diarrhea Laxative abuse Perspiration Excessive colas consumption 48

49. Potassium (K + ) Hypokalemia Causes Renal losses DKA Diuretics: thiazide, loop diuretics Drugs: amphotericin B, Cisplastin Hypomagnesemia Alkalosis Hyperaldosteronism Licorice ingestion Gitelman & Bartter syndrome 49

50. Potassium (K + ) Hypokalemia 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 50

51. Potassium (K + ) 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 51

52. Potassium (K + ) 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 52

53. Basic Metabolic Panel Na + Cl - BUN Ca ++ Glu Mg ++ K + HCO 3 -- Cr Phos -- 53

54. Bicarb (HCO 3 -- ) 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 54

55. Bicarb (HCO 3 -- ) Metabolic acidosis Anion gap: Na – (Cl + bicarb) Normal range: 12 +/- 2 55

56. Bicarb (HCO 3 -- ) Metabolic acidosis : causes for increase anion gap M U D P I L E S 56

57. Bicarb (HCO 3 -- ) Metabolic acidosis : causes for increase anion gap M ethanol U remia D KA P araldehyde or propylene glycol I soniazid L actic acidosis E thylene glycol S alicylates 57

58. Bicarb (HCO 3 -- ) Metabolic acidosis : causes for normal anion gap Diarrhea Pancreatic fistula Renal tubular acidosis or renal failure Intoxication: ammonium chloride, Acetazolamide, bile acid sequestrants, isopropyl alcohol Glue sniffing Toluene: 58

59. Bicarb (HCO 3 -- ) Metabolic acidosis Clinical presentation Chest pain, palpitation Kussmaul respirations Hyperkalemia Neuro: lethargy, stupor, coma, seizures Cardiac; arrhythmias, decreased response to Epinephrine, hypotension 59

60. Bicarb (HCO 3 -- ) Metabolic acidosis Treatment pH<7.1, risk of arrhythmias IV bicarb Dialysis 60

61. Bicarb (HCO 3 -- ) Metabolic alkalosis Causes Chloride responsive Compensated respiratory acidosis Diuretics  contraction alkalosis Vomiting Chloride resistant Retention of bicarb , shift hydrogen ion into IC space Alkalotic agents Hyperaldosteronism 61

62. Respiratory alkalosis pH>7.45, pCO2<35 Hgmm Causes: Hypoxic respiratory failure Salicylate intoxication Early sepsis Hepatic failure Arteficial hyperventilation Symptomes Decreased cerebral or coronary blood flow Neuromuscular excitability Therapy: Therapy of underlying disease Increasing the dead space

63. Respiratory acidosis pH<7.35, pCO2>45 Hgmm Cause: Respiratory failure Symptoms: Symptoms of metabolic acidosis + coma Therapy: Therapy of underlying disease Mechanical ventilation

64. Basic Metabolic Panel Na + Cl - BUN Ca ++ Glu Mg ++ K + CO 3 -- Cr Phos -- 64

65. Glucose Hypoglycemia Causes Complication of DM therapies Hyperinsulinemia Inborn errors of metabolism Alcohol Starvations Infections, organ failure 65

66. Glucose Hypoglycemia Clinical presentation Adrenergic Shakiness, anxiety, nervousness, palpitations, tachycardia Sweating, pallor, coldness, clamminess Glucagon Hunger, borborygmus, nausea, vomiting, abd. Discomfort Headache Neuroglycopenic AMS, fatigue, weakness, lethargy, confusion, amnesia. Ataxia, incoordination, slurred speech 66

67. Glucose Hypoglycemia Treatments 0.5-1 g/kg of dextrose 5-10 ml/kg of D10W 2-4 ml/kg of D25W Max 1 amp (50 g) 67

68. Basic Metabolic Panel Na + Cl - BUN Ca ++ Glu Mg ++ K + CO 3 -- Cr Phos -- 68

69. 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 Ca c = Ca m + [0.8 x (Alb n – Alb m )] 69

70. Calcium Roles: Coagulation Cellular signals Muscle contraction Neuromuscular transmission Controlled by parathyroid hormone and vitamin D 70

71. Calcium Hypercalcemia: Causes Excess parathyroid hormone, lithium use Excess vitamin D Malignancy Renal failure High bone turn over Prolonged immobilization Hyperthyroidism Thiazide use, vitamin A toxicity Paget’s disease Multiple myeloma 71

72. Calcium Hypercalcemia: Clinical 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 72

73. Calcium Hypercalcemia Treatments Fluid & diuretics Forced diuresis Loop diuretic Oral supplement: biphosphate or calcitonine Glucocorticoids Dialysis 73

74. Calcium Hypocalcemia Causes Eating disorder Hungry bone syndrome Ingestion: mercury , excessive Mg Chelation therapy EDTA Absent of PTH Ineffective PTH: CRF, absent or ineffective vitamin D, pseudohypoparathyroidism Deficient in PTH: acute hyperphos: TLS, ARF, Rhabdo Blood transfusions 74

75. Calcium Hypocalcemia: Clinical 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 75

76. Calcium Hypocalcemia: Treatments Supplements IV: gluconate or chloride with EKG change Oral calcium with vitamin D 76

77. Basic Metabolic Panel Na + Cl - BUN Ca ++ Glu Mg ++ K + CO 3 -- Cr Phos -- 77

78. 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 78

79. Magnesium Hypermagnesemia: Causes Hemolysis Renal insuficiency DKA, adrenal insufficiency, hyperparathyroidism, lithium intoxication 79

80. Magnesium Hypermagnesemia: Clinical 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 80

81. Magnesium Hypermagnesemia: Treatments Calcium infusion Diuretics Dialysis 81

82. Magnesium Hypomagnesemia Causes Alcoholism: malnutrition + diarrhea; Thiamine deficiency GI causes: Crohn’s, UC, Whipple’s disease, celiac sprue Renal loss: Bartter’s syndrome, postobstructive diuresis, ATN, kidney transplant DKA Drugs Loop and thiazide diuretics Abx: aminoglycoside, ampho B, pentamidine, gent, tobra PPI Others: digitalis, adrenergic, cisplastin, ciclosporine 82

83. Magnesium Hypomagnesemia: Clinical 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 83

84. Magnesium Hypomagnesemia: Treatments Oral or IV supplement Correct on going loss 84

85. Basic Metabolic Panel Na + Cl - BUN Ca ++ Glu Mg ++ K + CO 3 -- Cr Phos -- 85

86. 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 86

87. Phosphorus Hyperphosphatemia Causes Hypoparathyroidism Chronic renal failure Osteomalacia Presentations Ectopic calcification Renal osteodystrophy Treatments Dietary restriction Phosphate binder 87

88. Phosphorus Hypophosphatemia Causes Re-feeding syndrome Respiratory alkalosis Alcohol abuse Malabsorption 88

89. Phosphorus Hypophosphatemia Clinical presentation Muscle dysfunction and weakness: diploplia, low CO, dysphagia, respiratory depression AMS WBC dysfunction Instability of cell membrane  rhabdomyolysis Treatments supplementation 89

90. END