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Introduction to Fluid > Electrolyte Imbalance > Flashcards

Electrolyte Imbalance Flashcards

1
Q

Normal range of serum sodium level

A

135-145 mEq/L

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2
Q

Kidney Na excretion range

A

1-100 mEq/L

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3
Q

Cause of Hypovolemic Hyponatremia

A

Na loss > water loss

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4
Q

Renal loss of Na vs Extrarenal loss

A

Renal : Thiazide diuretics, > 20mEq/L

Extrarenal : GI, < 10mEq/L

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5
Q

Cause of Hypervolemic Hyponatremia

A

water gain > Na gain

impairment of renal free water excretion

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6
Q

Conditions associated with Hypervolemic Hyponatremia

A 
Edematous disorders
CHF
Cirrhosis,
Kidney failure
Nephrotic syndrome
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7
Q

Cause of Isovolumic Hyponatremia

A

Normal Na level
Increased water level

Dilutional hyponatremia

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8
Q

Conditions associated with Isovolumic Hyponatremia

A

Glucocorticoid insufficiency
Hypothyroidism
Syndrome of inappropriate ADH secretion (SIADH)

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9
Q

Clinical manifestation of Hyponatremia

A

Neurological (increased intracellular water)
Anorexia
Nausea
Weakness

Progressive cerebral edema
Lethargy
Confusion
Seizure
Coma
Death
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10
Q

Treatment of Hypovolemic Hyponatremia

A

Isotonic saline

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11
Q

Treatment of Isovolumic Hyponatremia

A

Water restriction

Demeclocycline (ADH antagonist)

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12
Q

Treatment of Hypervolemic Hyponatremia

A

Water restriction + Loop diuretics

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13
Q

Calculation of Na deficit

A

TBW X (desired [Na] - present [Na]

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14
Q

Excessively rapid correction problem

A

Demyelinating lesions in pons

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15
Q

Correcting rates for Hyponatremia of mild, moderate and severe symptoms

A

0.5, 1, 1.5 mEq/L/hr

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16
Q

Ways of achieving rapid correction of Hyponatremia

A

Loop diuretic + Isotonic saline

Intravenous Hypertonic saline

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17
Q

Anesthetic considerations of Hyponatremia

A

Decrease in MAC

Transurethral resection of prostate can absorb water (risk for rapid development of hyponatremia)

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18
Q

Major causes of Hypernatremia

A

water loss > Na loss

retention of Na

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19
Q

Most common cause of Hypernatremia with normal total body Na content

A

Diabetes insipidus (impairment of renal concentrating ability)

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20
Q

Cause of Hypernatremia with increased total body Na content

A

Hypertonic saline administration
Hyperaldosteronism
Cushing’s syndrome

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21
Q

Clinical manifestations of Hypernatremia

A

Cellular Dehydration (in brain esp)
Restlessness
Lethargy
Hyperreflexia

Rapid decrease in brain volume
Ruptured cerebral veins
Focal intracerebral hemorrhage
Subarachnoid hemorrhage

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22
Q

Treatment of Hypernatremia

A

5% dextrose in water + Loop diuretics

Isotonic fluid first in those with low Na content

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23
Q

Rapid correction of Hypernatremia problems

A

Seizure
Brain edema
Neurological damage
Death

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24
Q

Correction rate for Hypernatremia

A

0.5 mEq/L/hr

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25
Q

Anesthesia considerations of Hypernatremia

A

Increase MAC

Hypovolemia
Vasodilation
CVS depression –> Decrease Vd for IV drug
Decrease Cardiac output –> Increase uptake for Inhalational anesthetics

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26
Q

Normal serum Potassium level

A

3.5-5.5 mEq/L

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27
Q

Normal Potassium Balance (Input and Output)

A

Dietary intake - 80 mEq/d

Renal excretion - 70 mEq - Distal tubular secretion

GI excretion - 10 mEq

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28
Q

Extracellular and Plasma Potassium concentration determinant

A

Na+/K+ ATPase

Balance of K intake and excretion

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29
Q

Effect of Acidosis on K

A

H+ enters cells -> displaces K+

Serum K+ increases

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30
Q

Effect of Alkalosis on K

A

K+ moves in to cells to replace H+ out of cell

Serum K+ decreases

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31
Q

change in arterial pH : change in Plasma K

A

0.1 unit : 0.6 mEq/L

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32
Q

Effect of Aldosterone on Na and K

A

Na reabsorption

K excretion

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33
Q

Cause of Hypokalemia

A 
Excess renal/GI loss
Antibiotics
Renal tubular acidosis
ECF to ICF shift
Inadequate intake
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34
Q

Clinical Manifestation of Hypokalemia

A

Cardiovascular
Arrythmia

Neuromuscular
Weakness
Rhabdomyolysis

Renal
Polyuria

Hormonal
Decreased Insulin and aldosterone

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35
Q

ECG in Hypokalemia

A

Due to delayed ventricular repolarization

Flat and inverted T wave
Prominent U wave
Increased P amplitude
ST segment depression
PR interval prolongation
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36
Q

Treatment of Hypokalemia

A

Digoxin therapy
KCl (Oral) - safest
KCl (IV) - severe symptoms

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37
Q

Correction rate of Hypokalemia

A

Peripheral vein - 8mEq/h
Central vein - 10-20 mEq/h
Should not exceed 240 mEq/d

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38
Q

Anesthetic consideration

A

If normal - 3-3.5 mEq/L
If digoxin - 4 mEq/L

Glucose and Hyperventilation contraindicated

NMB reduced 25-50%

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39
Q

Maximum excretable K by the kidney

A

500 mEq/d

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40
Q

Causes of Hyperkalemia

A

Pseudo Hyperkalemia
Hemolysis, leukocytosis, thrombocytosis

Intercompartmental shift
Succinylcholine
Acidosis
Rhabdomyolysis

Decreased K excretion
Renal failure
Decreased mineralocorticoid activity

K sparing diuretics
Spironolactone

ACE1 Inhibitors
NSAID

41
Q

Clinical Manifestation of Hyperkalemia

A

Skeletal muscle weakness - > 8 mEq/L

Cardiac manifestation - > 7 mEq/L

42
Q

ECG in Hyperkalemia

A

Due to delayed depolarization

Peaked T wave
Widening of QRS
Prolongation of PR
Loss of P wave
Loss of R wave
ST depression
43
Q

Conditions that accentuate cardiac effect of Hyperkalemia

A

Hypocalcemia
Hyponatremia
Acidosis

44
Q

Treatment of Hyperkalemia

A

Beta agonist
Calcium (gluconate or chloride)
IV sodium bicarbonate (15 min)
IV glucose and insulin (1 hr)

45
Q

Anesthetic Considerations for Hyperkalemia

A

SUX and RL are contraindicated
Controlled, mild hyperventilation
Increased sensitivity to NMB

46
Q

Normal calcium intake and output balance

A

Dietary intake - 600-800 mg/d

Fecal excretion - 80%

Renal excretion - 50 - (100) - 300 mg/d

Reabsorption - Proximal tubule + Distal tubule (PTH)

47
Q

Plasma Calcium Concentration

A
  1. 5 - 10.5 mg/dl
  2. 1 - 2.6 mmol/L

50% - Free Ionized
40% - Protein bound
10 % - Anion bound

48
Q

Extracellular Ionized Calcium concentration regulation

A

Entry
Absorption from GI or Bone

Exit
Deposition into bone
Urinary excretion
Secretion into GI
Sweat formation
49
Q

Effect of PTH on Ca

A

Mobilization of Ca from bone
Enhance Ca reabsorption
Indirect increase in GI absorption (1,25 dihydroxycholecalciferol)

50
Q

Effect of Vitamin D on Ca

A

Augment GI absorption
Facilitate action of PTH
Augment Renal reabsorption

51
Q

Effect of Calcitonin on Ca

A

Inhibit bone reabsorption

Increases urinary Ca excretion

52
Q

Cause of Hypercalcemia

A

Hyperparathyroidism
Malignancy
Excessive Vitamin D intake

53
Q

Clinical Manifestation

A 
Ataxia
Irritability
Lethargy
Confusion
Cardiac arrest
Cardiac sensitivity to digitalis
54
Q

ECG of Hypercalcemia

A

Shorten ST

Shorter QT

55
Q

Treatment of Hypercalcemia

A

Rehydration (IV saline) + Loop diuretic
Calcitonin therapy
Dialysis (very severe Hypercalcemia, Kidney or Heart failure)

56
Q

Anesthetic Considerations of Hypercalcemia

A 
Avoid acidosis
Controlled ventilation 
Saline diuresis (to avoid hypovolemia)
57
Q

Cause of Hypocalcemia

A 
Hypoparathyroidism
Magnesium deficiency (Impair and antagonize PTH)
Hyperphosphatemia 
Vitamin D deficiency
Binding of Ca with citrate ions
58
Q

Clinical manifestations of Hypocalcemia

A

Paresthesia
Muscle spasms
Bone fracture
Decreased cardiac contractility (Heart failure, Hypotension)
Decreased responsiveness to digoxin and B-agonist

59
Q

ECG of Hypocalcemia

A

Prolonged QT

60
Q

Treatment of Hypocalcemia

A

IV Calcium chloride or gluconate

Chronic hypocalcemia - Oral calcium (CaCO3) and Vit D

61
Q

Anesthetic consideration of Hypocalcemia

A

Avoid fluid with bicarbonate or phosphate
Avoid alkalosis
Potentiate -ve inotropic effect of Barbs and volatile anesthetics
Inconsistent effect on NMB

62
Q

Distribution of Phosphorus in the body

A

Bone - 85%
Intracellular - 15%
Extracellular - 0.1

63
Q

Normal Phosphorus balance

A

Dietary intake - 800-1500 mg/d

GI absorption - 85%

Renal excretion

64
Q

Normal Plasma concentration

A
  1. 5 -4.5 mg/dl (6 in children)

0. 8 - 1.45 mmol/L

65
Q

Cause of Hyperphosphatemia

A

Excessive phosphorus intake
Decreased phosphorus excretion
Massive cell lysis

66
Q

Clinical manifestations of Hyperphosphatemia

A

Secondary effect on lowering Ca (deposition of CaPO4- in bone and tissue)

67
Q

Treatment of Hyperphosphatemia

A

Phosphate binding antacids

Aluminum hydroxide/carbonate

68
Q

Anesthetic consideration

A

Little

Exclusion of Secondary Hypocalcemia

69
Q

Cause of Hypophosphatemia

A

Negative phosphorus balance
Alkalosis
Carbohydrate ingestion
Insulin administration

Intercompartmental shift
  Large dose of antacids
  Severe burns
  Inadequate phosphorus administration 
    Hyperalimentation
    DKA
    Alcohol withdrawal
    Prolonged respiratory alkalosis
70
Q

Clinical manifestation of Hypophosphatemia

A 
Cardiomyopathy
Impaired oxygen delivery
Massive lysis of cells
Muscle myopathy
Metabolic acidosis
Hepatic dysfunction
71
Q

Treatment of Hypophosphatemia

A

Oral phosphorus + vitamin D

IV replacement therapy

72
Q

Why is Oral phosphorus replacement preferred from parenteral?

A

Risk of precipitation with calcium -> hypocalcemia
Hyperphosphatemia
Hypomagnesemia
Hypotension

73
Q

Anesthetic consideration for Hypophosphatemia

A

Avoid hyperglycemia and respiratory alkalosis
Monitoring of neuromuscular function when NMB administration
Post-op mechanical ventilation (muscle weakness)

74
Q

Distribution of Magnesium in the body

A

Bone - 67 %
Intracellular - 31%
Extracellular - 1-2%

75
Q

Physiologic effect of Mg

A

Decrease anesthetic requirement
Attenuate nociception
Blunt CVS response to laryngoscope and intubation
Potentiate NMB

76
Q

Suggested MoA of Mg

A

Altering CNS NT release
Moderating catecholamine release
Antagonizing the effect of Ca on vascular smooth muscle

77
Q

Use of Mg administration

A

Treatment of Mg deficiency
Pre-eclampsia and eclampsia
Digoxin-induced cardiac tachyarrhythmia
Status asthmaticus

78
Q

Normal Mg balance

A

Dietary intake - 20-30 mEq/d (240 -370 mg/d)

GI absorption - 30-40%

Renal excretion - 6-12 mEq/d

Proximal reabsorption - 25%
Distal reabsorption - 50%

79
Q

Factors that increase Mg reabsorption

A 
Hypomagnesemia 
PTH
Hypocalcemia
ECF depletion
Alkalosis
80
Q

Factors that increase Mg excretion

A 
Hypermagnesemia
Acute volume expansion
Hyperaldosteronism
Hypercalcemia
Ketoacidosis
Diuretic
Phosphate depletion
Alcohol ingestion
81
Q

Plasma Mg concentration

A

1.7-2.1 mEq/L (0.7-1 mmol/L)

Unbound and diffusible - 50-60%

82
Q

Causes of Hypermagnesemia

A 
Excessive Mg intake
Renal impairment (GFR < 30ml/min)
Adrenal insufficiency
Hypothyroidism
Lithium administration
83
Q

Clinical manifestations of Hypermagnesemia

A 
Neurologic, neuromuscular and cardiac manifestation
Hyporeflexia
Sedation
weakness
Respiratory depression
Vasodilation
Bradycardia
Myocardial depression
84
Q

ECG of Hypermagnesemia

A

Prolonged PR

Longer QRS

85
Q

Treatment of Hypermagnesemia

A

IV calcium
Loop diuretic + IV fluid replacement
Dialysis

86
Q

Anesthetic considerations of Hypermagnesemia

A

Potentiation of vasodilatory and negative inotropic properties of anesthetics
Reduced dosage of ND-NMB

87
Q

Cause of Hypomagnesemia

A 
Drugs that cause renal wasting of Mg
Ethanol
Diuretics
Aminoglycoside
Cyclosporin
88
Q

Clinical manifestations of Hypomagnesemia

A

Hypocalcemia (impaired PTH secretion)
Hypokalemia (Renal K wasting)
Electrical excitability and potentiation of digoxin toxicity

89
Q

ECG of Hypomagnesemia

A

Increased incidence of atrial fibrillation
Prolongation of PR
Prolonged QT

90
Q

Treatment of Hypomagnesemia

A

IV magnesium sulfate

91
Q

Cause of Hypochloremia

A 
GI loss
Respiratory loss
Excessive IV fluid
Loop and Thiazide diuretics
Aldosterone, Corticosteroids
Bicarbonates, Laxative
92
Q

Clinical manifestations of Hypochloremia

A 
Agitation, Irritablity 
Hyperactive DTR
Cramps
Shallow, slow respirations
Arrhythmias
93
Q

Treatment of Hypochloremia

A

Oral or IV replacement in NaCl or KCl

94
Q

Anesthetic consideration for Hypochloremia

A

Ammonium chloride for treatment of alkalosis

95
Q

Cause of Hyperchloremia

A 
Dehydration
Renal failure
Respiratory alkalosis
Salicylate toxicity
Hyperparathyroidism
Hyperaldosteronism
Hypernatremia
96
Q

Clinical manifestation of Hyperchloremia

A 
Kussmaul's respirations 
Weakness
Hypernatremia
Agitation
Tachycardia
Tachypnea
HTN
Edema
97
Q

Treatment of Hyperchloremia

A

Restore fluid, electrolyte and acid base balance

IV Lactated Ringer solution to correct acidosis

98
Q

Anesthetic consideration

A

Metabolic acidosis
Persistent tachypnea or hyperpnea -> atelectasis
Impairment of myocardial contraction
Avoid chloride containing solution

Introduction to Fluid (1 decks)

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