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Introduction to Fluid > Electrolyte Imbalance > Flashcards

Electrolyte Imbalance Flashcards

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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
Anesthesia considerations of Hypernatremia
Increase MAC Hypovolemia Vasodilation CVS depression --> Decrease Vd for IV drug Decrease Cardiac output --> Increase uptake for Inhalational anesthetics
26
Normal serum Potassium level
3.5-5.5 mEq/L
27
Normal Potassium Balance (Input and Output)
Dietary intake - 80 mEq/d Renal excretion - 70 mEq - Distal tubular secretion GI excretion - 10 mEq
28
Extracellular and Plasma Potassium concentration determinant
Na+/K+ ATPase Balance of K intake and excretion
29
Effect of Acidosis on K
H+ enters cells -> displaces K+ Serum K+ increases
30
Effect of Alkalosis on K
K+ moves in to cells to replace H+ out of cell Serum K+ decreases
31
change in arterial pH : change in Plasma K
0.1 unit : 0.6 mEq/L
32
Effect of Aldosterone on Na and K
Na reabsorption | K excretion
33
Cause of Hypokalemia
``` Excess renal/GI loss Antibiotics Renal tubular acidosis ECF to ICF shift Inadequate intake ```
34
Clinical Manifestation of Hypokalemia
Cardiovascular Arrythmia Neuromuscular Weakness Rhabdomyolysis Renal Polyuria Hormonal Decreased Insulin and aldosterone
35
ECG in Hypokalemia
Due to delayed ventricular repolarization ``` Flat and inverted T wave Prominent U wave Increased P amplitude ST segment depression PR interval prolongation ```
36
Treatment of Hypokalemia
Digoxin therapy KCl (Oral) - safest KCl (IV) - severe symptoms
37
Correction rate of Hypokalemia
Peripheral vein - 8mEq/h Central vein - 10-20 mEq/h Should not exceed 240 mEq/d
38
Anesthetic consideration
If normal - 3-3.5 mEq/L If digoxin - 4 mEq/L Glucose and Hyperventilation contraindicated NMB reduced 25-50%
39
Maximum excretable K by the kidney
500 mEq/d
40
Causes of Hyperkalemia
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
Clinical Manifestation of Hyperkalemia
Skeletal muscle weakness - > 8 mEq/L Cardiac manifestation - > 7 mEq/L
42
ECG in Hyperkalemia
Due to delayed depolarization ``` Peaked T wave Widening of QRS Prolongation of PR Loss of P wave Loss of R wave ST depression ```
43
Conditions that accentuate cardiac effect of Hyperkalemia
Hypocalcemia Hyponatremia Acidosis
44
Treatment of Hyperkalemia
Beta agonist Calcium (gluconate or chloride) IV sodium bicarbonate (15 min) IV glucose and insulin (1 hr)
45
Anesthetic Considerations for Hyperkalemia
SUX and RL are contraindicated Controlled, mild hyperventilation Increased sensitivity to NMB
46
Normal calcium intake and output balance
Dietary intake - 600-800 mg/d Fecal excretion - 80% Renal excretion - 50 - (100) - 300 mg/d Reabsorption - Proximal tubule + Distal tubule (PTH)
47
Plasma Calcium Concentration
8. 5 - 10.5 mg/dl 2. 1 - 2.6 mmol/L 50% - Free Ionized 40% - Protein bound 10 % - Anion bound
48
Extracellular Ionized Calcium concentration regulation
Entry Absorption from GI or Bone ``` Exit Deposition into bone Urinary excretion Secretion into GI Sweat formation ```
49
Effect of PTH on Ca
Mobilization of Ca from bone Enhance Ca reabsorption Indirect increase in GI absorption (1,25 dihydroxycholecalciferol)
50
Effect of Vitamin D on Ca
Augment GI absorption Facilitate action of PTH Augment Renal reabsorption
51
Effect of Calcitonin on Ca
Inhibit bone reabsorption | Increases urinary Ca excretion
52
Cause of Hypercalcemia
Hyperparathyroidism Malignancy Excessive Vitamin D intake
53
Clinical Manifestation
``` Ataxia Irritability Lethargy Confusion Cardiac arrest Cardiac sensitivity to digitalis ```
54
ECG of Hypercalcemia
Shorten ST | Shorter QT
55
Treatment of Hypercalcemia
Rehydration (IV saline) + Loop diuretic Calcitonin therapy Dialysis (very severe Hypercalcemia, Kidney or Heart failure)
56
Anesthetic Considerations of Hypercalcemia
``` Avoid acidosis Controlled ventilation Saline diuresis (to avoid hypovolemia) ```
57
Cause of Hypocalcemia
``` Hypoparathyroidism Magnesium deficiency (Impair and antagonize PTH) Hyperphosphatemia Vitamin D deficiency Binding of Ca with citrate ions ```
58
Clinical manifestations of Hypocalcemia
Paresthesia Muscle spasms Bone fracture Decreased cardiac contractility (Heart failure, Hypotension) Decreased responsiveness to digoxin and B-agonist
59
ECG of Hypocalcemia
Prolonged QT
60
Treatment of Hypocalcemia
IV Calcium chloride or gluconate | Chronic hypocalcemia - Oral calcium (CaCO3) and Vit D
61
Anesthetic consideration of Hypocalcemia
Avoid fluid with bicarbonate or phosphate Avoid alkalosis Potentiate -ve inotropic effect of Barbs and volatile anesthetics Inconsistent effect on NMB
62
Distribution of Phosphorus in the body
Bone - 85% Intracellular - 15% Extracellular - 0.1
63
Normal Phosphorus balance
Dietary intake - 800-1500 mg/d GI absorption - 85% Renal excretion
64
Normal Plasma concentration
2. 5 -4.5 mg/dl (6 in children) | 0. 8 - 1.45 mmol/L
65
Cause of Hyperphosphatemia
Excessive phosphorus intake Decreased phosphorus excretion Massive cell lysis
66
Clinical manifestations of Hyperphosphatemia
Secondary effect on lowering Ca (deposition of CaPO4- in bone and tissue)
67
Treatment of Hyperphosphatemia
Phosphate binding antacids | Aluminum hydroxide/carbonate
68
Anesthetic consideration
Little | Exclusion of Secondary Hypocalcemia
69
Cause of Hypophosphatemia
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
Clinical manifestation of Hypophosphatemia
``` Cardiomyopathy Impaired oxygen delivery Massive lysis of cells Muscle myopathy Metabolic acidosis Hepatic dysfunction ```
71
Treatment of Hypophosphatemia
Oral phosphorus + vitamin D | IV replacement therapy
72
Why is Oral phosphorus replacement preferred from parenteral?
Risk of precipitation with calcium -> hypocalcemia Hyperphosphatemia Hypomagnesemia Hypotension
73
Anesthetic consideration for Hypophosphatemia
Avoid hyperglycemia and respiratory alkalosis Monitoring of neuromuscular function when NMB administration Post-op mechanical ventilation (muscle weakness)
74
Distribution of Magnesium in the body
Bone - 67 % Intracellular - 31% Extracellular - 1-2%
75
Physiologic effect of Mg
Decrease anesthetic requirement Attenuate nociception Blunt CVS response to laryngoscope and intubation Potentiate NMB
76
Suggested MoA of Mg
Altering CNS NT release Moderating catecholamine release Antagonizing the effect of Ca on vascular smooth muscle
77
Use of Mg administration
Treatment of Mg deficiency Pre-eclampsia and eclampsia Digoxin-induced cardiac tachyarrhythmia Status asthmaticus
78
Normal Mg balance
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
Factors that increase Mg reabsorption
``` Hypomagnesemia PTH Hypocalcemia ECF depletion Alkalosis ```
80
Factors that increase Mg excretion
``` Hypermagnesemia Acute volume expansion Hyperaldosteronism Hypercalcemia Ketoacidosis Diuretic Phosphate depletion Alcohol ingestion ```
81
Plasma Mg concentration
1.7-2.1 mEq/L (0.7-1 mmol/L) Unbound and diffusible - 50-60%
82
Causes of Hypermagnesemia
``` Excessive Mg intake Renal impairment (GFR < 30ml/min) Adrenal insufficiency Hypothyroidism Lithium administration ```
83
Clinical manifestations of Hypermagnesemia
``` Neurologic, neuromuscular and cardiac manifestation Hyporeflexia Sedation weakness Respiratory depression Vasodilation Bradycardia Myocardial depression ```
84
ECG of Hypermagnesemia
Prolonged PR | Longer QRS
85
Treatment of Hypermagnesemia
IV calcium Loop diuretic + IV fluid replacement Dialysis
86
Anesthetic considerations of Hypermagnesemia
Potentiation of vasodilatory and negative inotropic properties of anesthetics Reduced dosage of ND-NMB
87
Cause of Hypomagnesemia
``` Drugs that cause renal wasting of Mg Ethanol Diuretics Aminoglycoside Cyclosporin ```
88
Clinical manifestations of Hypomagnesemia
Hypocalcemia (impaired PTH secretion) Hypokalemia (Renal K wasting) Electrical excitability and potentiation of digoxin toxicity
89
ECG of Hypomagnesemia
Increased incidence of atrial fibrillation Prolongation of PR Prolonged QT
90
Treatment of Hypomagnesemia
IV magnesium sulfate
91
Cause of Hypochloremia
``` GI loss Respiratory loss Excessive IV fluid Loop and Thiazide diuretics Aldosterone, Corticosteroids Bicarbonates, Laxative ```
92
Clinical manifestations of Hypochloremia
``` Agitation, Irritablity Hyperactive DTR Cramps Shallow, slow respirations Arrhythmias ```
93
Treatment of Hypochloremia
Oral or IV replacement in NaCl or KCl
94
Anesthetic consideration for Hypochloremia
Ammonium chloride for treatment of alkalosis
95
Cause of Hyperchloremia
``` Dehydration Renal failure Respiratory alkalosis Salicylate toxicity Hyperparathyroidism Hyperaldosteronism Hypernatremia ```
96
Clinical manifestation of Hyperchloremia
``` Kussmaul's respirations Weakness Hypernatremia Agitation Tachycardia Tachypnea HTN Edema ```
97
Treatment of Hyperchloremia
Restore fluid, electrolyte and acid base balance IV Lactated Ringer solution to correct acidosis
98
Anesthetic consideration
Metabolic acidosis Persistent tachypnea or hyperpnea -> atelectasis Impairment of myocardial contraction Avoid chloride containing solution

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