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Fluids and Electrolytes
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Total Body Water
60% Male, 50% Female Less as we age, because greater proportion of fat
TBW
Extracellular Intracellular
Plasma Interstitial
66%33%
8% 25%
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Body Fluid Compartments:
ICF:ICF:55%~75%55%~75%
IntravascularIntravascularplasmaplasma
ExtravascularExtravascularInterstitial Interstitial
fluidfluid
TBWTBW
ECFECF
3/4
1/4
Most concentrated in skeletal muscle
TBW=0.6xBW ICF=0.4xBW ECF=0.2xBW
2/3
1/3
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Distribution of Solutes
Extracellular Intracellular
Na+ 142 Na+ 10
K+ 4 K+ 140
Cl- 110 Cl- 3
HCO3- 24 HCO3
- 10
Inorganic - 12 Inorganic - 137
Glucose 3 Glucose 2.5
Osmols 300 Osmols 300
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Plasma osmolarity 280-295 (2 x Na) + (glucose/18) + (BUN/2.8)
Which one of the following is not needed to calculate osmolarity? Potassium, sodium, glucose, urea, chloride
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Maintenance fluid 4cc/kg/day for 1st 10kg 2cc/kg/day for 2nd 10kg 1cc/kg/day for every kg after Maintenance fluid of choice for adult
D5 ½ NS w/ 20 mEq K Maintenance fluid of choice for child
D5 ¼ NS w/ 20 mEq K
Insensible fluid losses 10 cc/kg/day, 75% skin, 25% respiratory
Open abdominal operations Fluid loss 0.5-1 L/hr
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In the pediatric patient, what is the recommended initial fluid challenge?
10 ml/kg lactated Ringer’s 20 ml/kg lactated Ringer’s 50 ml/kg lactated Ringer’s 10 ml/kg high molecular weight dextran
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GI fluid secretion Stomach 1-2 L/day Biliary syst 0.5-1 L/day Pancreas 0.5-1 L/day SB 0.5-1 L/day Saliva 1-1.5 L/day
Na requirement 1-2 mEq/kg/day
K+ requirement 0.5-1 mEq/kg/day
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GI losses Sweat – hypotonic Saliva – K+ Stomach – HCL Pancreas – Bicarb Bile – Bicarb SB – Bicarb and K+ LB – K+
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Metabolic acidosis Anion gap:
Phosphates, sulfates, lactate, keto acids, proteins 10-12 mEq/L Na – (HCO3 + Cl)
Anion gap acidosis MUDPILES Methanol, uremia, dka, paraldehyde, isoniazide, lactatemia, ethylene
glycol, salicylates Normal anion gap
usually loss of Na/HCO3
Metabolic alkalosis Vomiting, NG tube: hypochloremic, hypokalemic, metabolic alkalosis, paradoxical
aciduria
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IVF Solutions
LR 130 mEq Na 109 mEq Cl 28 mEq Lactate 4 mEq K 3 mEq Ca
NS 154 mEq Na 154 mEq Cl
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Hyponatremia
Mild 130-138
Moderate 120-130 HA or lethargy 2o swelling intracranial cells
Severe < 120
Risk Seizure, Coma <110
Risk of death from cerebral swelling
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Acute Hyponatremia Evolves in few hours Make sure to resuscitate with iso-osmotic fluid Water Intoxication Forced Diuresis (loop, mannitol, DKA) Cerebral Salt Wasting
Chronic Hyponatremia SIADH Renal Disease Adrenal Disease (rare)
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Treatment
Correct Na deficit slowly Max rate of sodium correction
Should not exceed 0.25 mEq/L/hr Or 8 mOsm/kg H2O per day
Need to Avoid Central Pontine Myelinolysis
Permanent neurologic disorder Spastic quadriparesis Pseudobulbar palsy Depressed consciousness
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Hypernatremia
Most common cause of Hypertonicity Moderate
146-159 Severe
>160
Altered LOC Seizure Coma Sudden dehydration can lead to intracerebral
hemorrhage
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Causes of Hypernatremia
DI Greater than 500 mL/hr hypotonic urine Continual production of dilute urine (urine osmol <
200) while serum osmol >300 Central
Hypothalamus can’t produce vasopressin Nephrogenic
Renal tubules can’t respond to vasopressin
EtOH intoxication Excessive losses of hypotonic fluids
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Which one of the following meds is not capable of causing DI? Desmopressin Lithium Demeclocycline Amphotericin B Glyburide
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Treatment of Hypernatremia
IV or oral administration of fluid Determine Free Water Deficit 0.6 or 0.5 x (wt in kg) x [(serum Na/140)-1]
Slow correction Brain swelling 10 mEq/day unless symptomatic
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Hyperkalemia Defined by K > 5.0
> 6.0 Cardiac Arrhythmias Elevated T waves
>7.0 P wave amplitude decreases PR segment increases QRS complex widens
>8.0 Lethal arrhythmias (asystole, V Fib, pulseless
idioventricular rhythm)
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Causes of Hyperkalemia
Renal Failure Medication
K sparing diuretics Succinylcholine
Reperfusion injury Burn
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Treatment of Hyperkalemia
C Calcium
B Bicarb
I Insulin
G Glucose
K Kayexalate
F Furosemide
A Aldosterone
L L
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Hypokalemia
K < 3.5 Fatigue Weakess Ileus
K < 2.0 Flaccid paralysis Respiratory compromise
Cardiac Arrhythmias Depressed T waves U waves Atrial tachycardia w/ or w/out block AV dissociation Ventricular tachycardia Ventricular fibrillation
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Which is the correct electrolyte makeup of plasma? Na: 150 K: 4 Cl: 103 HCO3: 24 Na: 140 K: 4 Cl: 98 HCO3: 26 Na: 140 K: 4 Cl: 103 HCO3: 24 Na: 145 K: 4 Cl: 103 HCO3: 28
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Normal Saline contains 154 meq of Na & Cl
LR contains Na 130 Cl 109 K 4 Ca 2.7 and bicarb 28
Cannot transfuse blood with LR because: calcium in Ringer's lactate solution could
overwhelm the chelating capacities of the citrate in stored blood, resulting in clot formation.
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Calcium
Normal level? 8.5 to 10.5 mg/dL
Total calcium accounts for 3 forms of calcium?
Protein-bound calcium Diffusible calcium complexed to anions (bicarbonate,
phosphate, and acetate) Freely diffusible
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Calcium continued …
Ionized calcium Biochemically active species Comprises ~45% of total serum calcium
Protein bound calcium 80% bound to albumin Acidemia decreases calcium binding to albumin
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What factors affect calcium levels? PTH Calcitonin Vitamin D
PTH effects? Activates osteoclasts Stim tubule cells in the proximal nephron to absorb
calcium and excrete phosphates Works with vit D to enhance absorption of calcium from
the gut lumen Conversion of dietary vit D to 1, 25-
dihydroxycholecalciferol
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VITAMIN D SYNTHESIS
SKIN LIVER KIDNEY
7-DEHYDROCHOLESTEROL
VITAMIN D3
VITAMIN D3
25(OH)VITAMIN D
h 25-HYDROXYLASE
25(OH)VITAMIN D
1,25(OH)2 VITAMIN D
(ACTIVE METABOLITE)
1-HYDROXYLASE
TISSUE-SPECIFIC VITAMIN D RESPONSES
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FUNCTION OF VITAMIN D TISSUE SPECIFICITY
GUT STIMULATE TRANSEPITHELIAL TRANSPORT OF CALCIUM AND
PHOSPHATE IN THE SMALL INTESTINE (PRINCIPALLY DUODENUM)
BONE STIMULATE TERMINAL DIFFERENTIATION OF OSTEOCLASTS STIMULATE OSTEOBLASTS TO STIMULATE OSTEOCLASTS TO
MOBILIZE CALCIUM PARATHYROID
INHIBIT TRANSCRIPTION OF THE PTH GENE (FEEDBACK REGULATION)
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Hypercalcemia
Symptoms Fatigue, weakness, anorexia, n/v Pain, polydipsia, polyuria, stones Stupor, coma
Critical level: 16-20mg/ml
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Hypercalcemia cont.
Causes Hyperparathyroidism (unregulated PTH secretion) Malignancies
PTH-related peptide- share 8 of the first 13 amino acids with
PTH Nonhormonal mechanisms
- direct invasion with activation of osteoclast activity via cytokines (IL-1, TNF, IL-6)
Drugs Thiazide diuretics Extreme doses of Vit A & Vit D
Immobility Young, normally active patients with high bone turnover
PTHrP Very high hypercalcemia, suppressed PTH
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One of the first cancers recognized to cause hypercalcemia
MULTIPLE MYELOMA
Mediated by family of cytokines causing osteoclast activation Hypercalcemia, suppressed PTH
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Hypercalcemia cont.
CHIMPANZEES Calcium excess (administration) Hyperparathyroidism Immobility / iatrogenic Metastasis / milk-alkali syndrome Paget’s disease Addison’s disease Neoplasms Excess vit D Excess vit A Sarcoidosis
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Hypercalcemia Treatment
Saline infusion to expand ECW loop diuretic Renal failure hemodialysis Correct primary problem
PTH excision of diseased tissue Drugs Malignancy excision, XRT, or chemotherapy
Long term Bisphosphonate
Reduce osteoclast-mediated release of calcium from bone Given as long term prophylaxis in pts with metastatic cancer
Calcitonin Induces renal excretion of calcium Suppresses osteoclast bone reabsorption
Long term tx tachyphylaxis Chelating agents (EDTA or phosphate salts)
Rarely indicated
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Hypocalcemia
Symptoms Numbness, paresthesias of the distal extremities and
circumoral region Chvostek sign
- a twitch of facial muscles elicited by tapping gently on the facial nerve
Trousseau’s sign
- carpopedal spasm induced by 3 min of inflation of a BP cuff above the brachial artery
Painful muscle spasms Cardiac dysfunction
Impaired contractility Prolonged QT interval complete heart block or v-fib
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Hypocalcemia cont.
Causes Parathyroid surgery Tumor lysis syndrome Severe pancreatitis Rapid infusion of citrate with blood products Dietary deficiencies, short gut syndrome Impaired vit D conversion
Available forms of calcium replacement? CaCl2
10% solution 272 mg calcium (13.6 mmol) Ca gluconate
10% solution 90mg calcium (4.5 mmol)
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Hypocalcemia cont.
Tumor lysis syndrome? Constellation of electrolyte abnormalities that occur
when antineoplastic therapy causes a sudden surge in tumor cell death and release of cytosol contents
Assoc with: solid tumors and lymphoma
Electrolyte abnormalities Hypocalcemia Hyperphosphatemia Hyperuricemia Hyperkalemia
Acute renal failure prevents spontaneous correction
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Elderly alcoholic man who takes loop diuretics is seen in ER with sxs of hypocalcemia. They are unable to correct the deficit. What else should they correct?
Ca K Mg Phos Na
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Magnesium
Normal plasma concentration 1.4 to 2.0 mEq/L
Hypermagnesemia symptoms appear when Mg > 6 mg/dL. altered mental status, lethargy, depressed DTR, flaccid paralysis. Respiratory depression
Treatment: Loop diuretics. Calcium, 10 – 20 meq, can reverse the clinical signs.
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Hypomagnesemia Gastrointestinal loss:
Diarrhea, malabsorption, vomiting, biliary fistulas Urinary loss:
Diuresis or renal tubular dysfunctions. Drugs: cisplatin, cyclosporin, loop diuretics, amphotericin B,
aminoglycosides. Shifting into cells
Acute MI, alcoholic withdrawal, glucose injection.
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Hypomagnesemia cont.
Treatment Intravenous magnesium sulfate (MgSO4)
Sustained therapy req for severe ↓Mg (<1.0 mEq/L) Due to slow equilibration of extracellular Mg with
intracellular stores