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FUNDAMENTALS OF FLUID AND ELECTROLYTE BALANCE

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D5 NS with KCL 20 meq/L running at 100 ml/hr. MAINTENANCE ... Isotonic hyponatremia (factitious) Hypertonic hyponatremia (dilutional) Hypotonic hyponatremia ... – PowerPoint PPT presentation

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Title: FUNDAMENTALS OF FLUID AND ELECTROLYTE BALANCE


1
FUNDAMENTALS OF FLUID AND ELECTROLYTE BALANCE
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FLUID REQUIREMENTS
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FLUID CONTENT OF THE BODY
  • Varies with age, sex, adipose tissue
  • Females 45-50 TBW
  • Males 50-60 TBW
  • Infants 77 TBW

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BODY FLUID COMPARTMENTS
  • RULE OF THIRDS
  • Intracellular 2/3 (40 TBW)
  • Extracellular 1/3 (20 TBW)
  • Interstitial Lymph 2/3 (15 TBW)
  • Intravascular 1/3 (5 TBW)

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ELECTROLYTES IN BODY FLUID COMPARTMENTS
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SOLUTES
  • Non-electrolytes
  • Dextrose
  • Urea
  • Creatinine
  • Electrolytes
  • Anions
  • Cations

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IV FLUID DISTRIBUTION IN BODY COMPARTMENTS
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MAINTENANCE vs. REPLACEMENT
  • Maintenance
  • Provide normal daily requirements Water 2.5 L
  • Sodium ½ or ¼ NS
  • KCl 40-60 meq/L
  • Example
  • D5 ½ NS with KCL 20 meq/L running at 100 ml/hr

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MAINTENANCE vs. REPLACEMENT
  • Replacement
  • Replace abnormal losses with a fluid and
    electrolytes similar to that which was lost.

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OSMOLALITY
  • Definition Concentration of particles
    (osmotically active) in solution. It is usually
    expressed in millosmoles of solute per kg of
    solution.
  • Osmolality is independant of valence.
  • Osmolality (mOsm/Kg) of dilute solutions
    approximate osmolarity (mOsm/L)
  • Plasma 280-300 mOsm/Kg
  • Same in all body compartments
  • Water distribution

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Normal Laboratory Values
  • Sodium 135-145 meq/L
  • Potassium 3.5-5.0 meq/L
  • Chloride 95-105 meq/L
  • Bicarbonate 22-28 meq/L
  • Calcium 9-11 mg/dL
  • Phosphate 3.2-4.3 mg/dL
  • Glucose 70-110 mg/dL
  • BUN 8-18 mg/dL
  • Creatinine 0.6-1.2 mg/dL
  • Osmolality (P) 280-295 mOsm/kg
  • Osmolality (U) 50-1200 mOsm/kg

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ELECTROLYTE DISORDERSSODIUM
  • JO is a 58 year-old male with cirrhosis of the
    liver due to ethanol abuse. Physical examination
    reveals ascites.
  • Baseline lab is as follows
  • Na 128, K 3.8, Cl 95, CO2 24
  • JO is to be started on TPN, Should we request
    additional sodium to correct his hyponatremia?

20
ELECTROLYTE DISORDERSSODIUM
  • Primary extracellular cation
  • Hyponatremia
  • Excess of TB water
  • Decrease in TB sodium
  • Serum sodium primarily reflects water balance,
    not sodium balance.

21
ELECTROLYTE DISORDERSSODIUM
  • Isotonic hyponatremia (factitious)
  • Hypertonic hyponatremia (dilutional)
  • Hypotonic hyponatremia

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ELECTROLYTE DISORDERSSODIUMHypertonic
Hyponatremia

Extracellular Fluid BS 400 mg/dl Na
Intracellular Fluid Water
23
ELECTROLYTE DISORDERSHypotonic Hyponatremia

24
ELECTROLYTE DISORDERSSODIUM
  • JO is a 58 year-old male with cirrhosis of the
    liver due to ethanol abuse. Physical examination
    reveal ascites.
  • Baseline lab is as follows
  • Na 128, K 3.8, Cl 95, CO2 24
  • JO is to be started on TPN, Should we request
    additional sodium to correct his hyponatremia?
  • JOs is in an edematous state. He has an excess
    of TB water and sodium. The appropriate
    treatment is water and sodium restriction. He
    should also receive diuretic treatment. The drug
    of choice is Aldactone (spironolactone), an
    aldosterone antagonist.

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ELECTROLYTE DISORDERSModel for Distribution and
Elimination of Intracellular Ions

Intake
K Phos Mg ICF
ECF
Stomach Intestine
Renal Losses
GI (stool) Losses
26
ELECTROLYTE DISORDERSPOTASSIUM
  • Primary intacellular cation
  • Hypokalemia Causes
  • Decreased dietary intake
  • Redistribution
  • Insulin
  • Metabolic Alkalosis
  • Dehydration

27
ELECTROLYTE DISORDERSPOTASSIUMMetabolic
Alkalosis and Hypokalemia

Extracellular Fluid K
Intracellular Fluid H
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ELECTROLYTE DISORDERSPOTASSIUM
  • Hypokalemia Causes
  • Increased Urinary or GI Losses
  • Diuretics
  • NG Suction
  • Diarrhea

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ELECTROLYTE DISORDERSPOTASSIUM
  • Drugs which may cause hypokalemia
  • Urinary wasting aminoglycosides, amphotericin B,
    corticosteroids, diuretics, levodopa, nifedipine,
    penicillins, rifampin
  • Gastrointestinal losses laxatives
  • Redistribution Beta-2 agonists, lithium

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ELECTROLYTE DISORDERSPOTASSIUM
  • Hypokalemia Treatment/Estimation of Deficit
  • If serum K gt 3meq/L
  • 100-200 meq required per each change in serum K
    of 1 meq/L
  • If serum K lt 3 meq/L
  • 200-400 meq required per each change in serum K
    of 1 meq/L

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ELECTROLYTE DISORDERSPOTASSIUM
  • Hypokalemia Estimation of Deficit
  • If serum K gt 3meq/L
  • 100-200 meq required per each change in serum K
    of 1 meq/L
  • If serum K lt 3 meq/L
  • 200-400 meq required per each change in serum K
    of 1 meq/L
  • Example Serum K 2.5 How much K is required to
    correct serum K to 4.0?
  • Step 1
  • To increase from 2.5 to 3.0 200-400 meq X
    0.5100-200meq
  • Step 2
  • To increase from 3.0 to 4.0 100-200 meq X
    1.0100-200meq

  • Total200-400meq

32
ELECTROLYTE DISORDERSPOTASSIUM Hypokalemia
Treatment
33
ELECTROLYTE DISORDERSPOTASSIUM
  • Mrs D. is a 62 year-old female who is having an
    acute exacerbation of Crohns disease. She
    complains to you of severe and frequent diarrhea
    over the last four days. She experiences
    dizziness when she stands. Your physical
    examination reveals dry mucous membranes. In the
    supine position her BP110/65 and in the upright
    position her BP90/45 and her pulse140. Your
    lab values are as follows
  • Na 132, K 2.9, Cl 92, CO2 31, BUN 25, Cr 1.0
  • Discuss Mrs. Ds fluid and electrolyte problems.

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ELECTROLYTE DISORDERSCase Study Hypokalemia
  • Mrs D. is a 62 year-old female who is having an
    acute exacerbation of Crohns disease. She
    complains to you of severe and frequent diarrhea
    over the last four days. She experiences
    dizziness when she stands. Your physical
    examination reveals dry mucous membranes. In the
    supine position her BP110/65 and in the upright
    position her BP90/45 and her pulse140. Your
    lab values are as follows
  • Na 132, K 2.9, Cl 92, CO2 31, BUN 25, Cr 1.0
  • Mrs Ds has extracellular volume depletion due
    to prolonged diarrhea. The ECVD is supported by
    her physical assessment and postural hypotension
    and her BUN/Cr is gt 201. The diarrhea has
    resulted in a loss of fluid and sodium chloride.
    Some potassium was lost directly in the stools,
    but the main cause of her hypokalemia is her ECVD
    which has induced a metabolic alkalosis
    (contraction alkalosis.) The alkalosis
    contributed to her hypokalemia by two mechanisms.
    Some potassium has moved to the intracellular
    compartment but much of it has been lost in the
    urine where potassium wasting occurs secondary to
    chloride deficit. Administration of Normal
    Saline with Potassium Chloride will correct her
    fluid and electrolyte problems (and alkalosis.)

35
ELECTROLYTE DISORDERSPOTASSIUM
  • Hyperkalemia Causes
  • Decreased Renal Excretion
  • CRF and ARF
  • Drug induced
  • K-sparing diuretics (spironolactone,
    triamterine, amiloride)
  • Angiotensin converting enzyme inhibitors
  • NSAIDS

36
ELECTROLYTE DISORDERSPOTASSIUM
  • Hyperkalemia Causes
  • Redistribution
  • Trauma, burns
  • Acidosis
  • Hyperosmolar states
  • Increased intake
  • Salt substitutes
  • Blood transfusions
  • K salts of antibiotics

37
ELECTROLYTE DISORDERSPOTASSIUMMetabolic
Acidosis and Hyperkalemia

Extracellular Fluid H
Intracellular Fluid K
38
ELECTROLYTE DISORDERSPOTASSIUM
  • Hyperkalemia Treatment
  • Potassium Antagonist
  • Calcium Chloride
  • Redistribution
  • Insulin dextrose
  • Sodium bicarbonate
  • Cationic binding resins
  • Kayexalate (polystyrene sulfonate)
  • Renal Elimination/dialysis

39
ELECTROLYTE DISORDERSMAGNESIUM
  • Hypomagnesemia Causes
  • Decreased Intake
  • Malnutrition
  • Alcoholism
  • Decreased Absorption
  • Increased Losses
  • GI losses
  • Renal losses

40
ELECTROLYTE DISORDERSMAGNESIUM
  • Drug Induced Hypomagnesemia
  • GI Losses
  • Laxatives
  • Renal Losses
  • Diuretics, cisplatin, aminoglycosides,
    amphotericin B

41
ELECTROLYTE DISORDERSMAGNESIUM
  • Hypomagnesemia Treatment
  • IV Magnesium Sulfate
  • Replace over several days
  • Renal threshold for reabsorption of Mg
  • 1 mEq/kg on day 1
  • 0.5 mEq/kg on days x 3-5 days
  • Oral replacement
  • Mylanta

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ELECTROLYTE DISORDERSMAGNESIUM
  • Hypermagnesemia Causes
  • Exogenous ingestion
  • Impaired renal excretion
  • Treatment Eliminate exogenous source of Mg

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ELECTROLYTE DISORDERSPHOSPHOROUS
  • Hypophosphatemia usually asymptomatic until lt1
    mg/dL
  • Causes
  • Impaired absorption
  • Aluminum or calcium binding
  • Redistribution
  • Respiratory alkalosis
  • Glucose insulin
  • Increased Excretion

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ELECTROLYTE DISORDERSPHOSPHOROUS
  • Hypophosphatemia Treatment
  • Oral Fleets Phosphosoda
  • IV Replace cautiously

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ELECTROLYTE DISORDERSPHOSPHOROUS
  • Hyperphosphatmeia Causes
  • Renal impairment
  • Increased intake
  • Treatment
  • Phosphate binders Alternagel, Amphojel,
    Calcium Suppliments

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ELECTROLYTE DISORDERSPHOSPHOROUS
  • M.T. is a 55 year-old female with a history of
    chronic renal failure who is admitted to the SICU
    following a motor vehicle accident. She is
    started on a TPN solution with minimal K, no Mg
    and no Phos. She also receives Mylanta II 30 ml
    per NG tube every four hours. Although her
    baseline labs were normal on day six her labs are
    as follows
  • K 4.3, Mg 2.6, Phos 1.6
  • What role did the antacid play in her electrolyte
    abnormalities?
  • What role did the TPN play?

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ELECTROLYTE DISORDERSPHOSPHOROUS
  • M.T. is a 55 year-old female with a history of
    chronic renal failure who is admitted to the SICU
    following a motor vehicle accident. She is
    started on a TPN solution with minimal K, no Mg
    and no Phos. She also receives Mylanta II 30 ml
    per NG tube every four hours. Although her
    basline labs were normal on day six her labs are
    as follows
  • K 4.3, Mg 2.6, Phos 1.6
  • M.Ts K is normal, but she has hypermagnesemia
    and hypophosphatemia. The antacid contributed to
    both of these abnormalities. It provided a
    significant source of Mg this patient with
    impaired excretion. Also the aluminum in the
    antacid acted a phosphate binder contributing to
    the hypophosphatemia.
  • The TPN could have contributed to the
    hypophosphatemia by inducing an intracellular
    shift of phosphate (refeeding.) The potassium
    probably remained normal because some was being
    provided. Mg was being provided enterally.

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