20336123 body fluid electrolyte management
TRANSCRIPT
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The recognition and
management of fluid,
electrolyte, and related acid-
base problems are common
challenges on the surgical
service.
Lawrence, Essentials of General Surgery
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Goals
Introduce concept of total body fluids
Introduce types of crystalloids
Intrduce electrolytes disturbances & their
treatment strategies.
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Body Fluids
Intercellular
Intravascular
Interstitial4%
40%
Body Water = 60% of a patients body weight
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Fluid Requirements
typically 35 mL/kg/day
insensible loss = 700 mL/day or 0.2
cc/kg/day for every 1 C > 37
1-10 kg = 100 mL/kg/day {4mL/kg/hr}
11-20 kg = 50 mL/kg/day {2mL/kg/hr}
> 21 kg = 20 mL/kg/day {1mL/kg/hr}
Trick for hourly maintenance = 40 + weight (kg)
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Serum Values of Electrolytes
Cations Concentration, mEq/LSodium 135 - 145
Potassium 3.5 - 4.5
Calcium 4.0 - 5.5
Magnesium 1.5 - 2.5
Anions
Chloride 95 - 105
CO2 24 - 30
Phosphate 2.5 - 4.5
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Electrolyte in body fluid
ECF: Na+ Cl- HCO3-, mainly
maintained by Na+.
ICF: K + Mg2 + HPO42- Pr-,
mainly maintained by K+.
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Composition of Fluids
plasma interstitial intracellular
CationsNa 140 146 12K 4 4 150
Ca 5 3 10Mg 2 1 7
AnionsCl 103 104 3
HCO 24 27 10SO4 1 1 -HPO4 2 2 116Protein 16 5 40
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Daily Requirements for
Electrolytes
Sodium: 1-2 mEq/kg/dPotassium: 0.5-1 mEq/kg/d
Calcium: 800 - 1200 mg/d
Magnesium: 300 - 400 mg/dPhosphorus: 800 - 1200 mg/d
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Interstitial fluid
Interstitial fluid (ortissue fluid, orintercellular fluid) is asolution which bathes
and surrounds the cellsof multicellular animals.It is the maincomponent of theextracellular fluid ,
which also includesplasma andtranscellular fluid.
http://en.wikipedia.org/wiki/Extracellular_fluidhttp://en.wikipedia.org/wiki/Blood_plasmahttp://en.wikipedia.org/wiki/Transcellular_fluidhttp://en.wikipedia.org/wiki/Image:Illu_capillary_microcirculation.jpghttp://en.wikipedia.org/wiki/Transcellular_fluidhttp://en.wikipedia.org/wiki/Blood_plasmahttp://en.wikipedia.org/wiki/Extracellular_fluid -
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How to differentiate function and non-function interstitial fluids
Function: Taking part in modulatingthe balance of body fluids.
Non-function: Fluids in cavity in
normal status.Including cerebrospinal ,joint, pericardium and abdominal
cavity fluids.
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Third Space
Definition:
Pathophysiologically, relatively nonfunctional
extra-cellular fluid. Mainly for the change of
quantity of functional and nonfunctional
ECF.
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Distribution:
exudates in burns; ascites; soft tissue
injuries. bowel wall; peritoneum; infected
lesions.
Attention:not confused with the nonfunctioning
components from interstitial fluid.
Third Space
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Control of Volume
Kidneys maintain constant volume andcomposition of body fluids
Filtration and reabsorption of Na
Regulation of water excretion in response toADH (antidiuretic hormone)
Water is freely diffusible
Movement of certain ions and proteins betweencompartments restricted
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The Concept of Osmotic
Pressure
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Osmotic pressure
Osmotic pressure is thehydrostaticpressureproduced by a solutionon a space, separated
from a solvent, by asemipermeablemembrane due to adifferential in theconcentrations of solute.
Osmoregulation is thehomeostasis mechanismof an organism to reachbalance in osmoticpressure.
http://en.wikipedia.org/wiki/Fluid_staticshttp://en.wikipedia.org/wiki/Pressurehttp://en.wikipedia.org/wiki/Differentially_permeable_membranehttp://en.wikipedia.org/wiki/Differentially_permeable_membranehttp://en.wikipedia.org/wiki/Osmoregulationhttp://en.wikipedia.org/wiki/Homeostasishttp://upload.wikimedia.org/wikipedia/commons/7/76/Osmotic_pressure_on_blood_cells_diagram.svghttp://en.wikipedia.org/wiki/Homeostasishttp://en.wikipedia.org/wiki/Osmoregulationhttp://en.wikipedia.org/wiki/Differentially_permeable_membranehttp://en.wikipedia.org/wiki/Differentially_permeable_membranehttp://en.wikipedia.org/wiki/Pressurehttp://en.wikipedia.org/wiki/Fluid_statics -
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water
water
Semi-permeable membrane
Anion and Cation as well as non-electrolyte particles
Pressure leading to the shift of water
through semi-permeable membrane
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Osmotic potential
Osmotic potential is the opposite ofwater potential withthe former meaning the degree to which a solvent (usuallywater) would want to stay in a liquid.
Hypertonicity is a solution that causes cells to shrink. Itmay or may not have a higher osmotic pressure than the
cell interior since the rate of water entry will depend uponthe permeability of the cell membrane.
Hypotonicity is a solution that causes cells to swell. It mayor may not have a lower osmotic pressure than the cellinterior.since the rate of water entry will depend upon the
permeability of the cell membrane. Isotonic is a solution that produces no change in cell
volume.
http://en.wikipedia.org/wiki/Water_potentialhttp://en.wikipedia.org/wiki/Tonicityhttp://en.wikipedia.org/wiki/Tonicityhttp://en.wikipedia.org/wiki/Tonicityhttp://en.wikipedia.org/wiki/Tonicityhttp://en.wikipedia.org/wiki/Tonicityhttp://en.wikipedia.org/wiki/Tonicityhttp://en.wikipedia.org/wiki/Water_potential -
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Definition
the number of osmotically active particles
or ions per unit volume.
Unit :
milliosmoles per liter mOsm / L
The Concept of Osmotic
Pressure
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Normal Range =290~310mOsm/L
cation mmol/L anion mmol/L
Na
K
Ca
Mg
142
5
2.5
1.5
HCO3
Cl
HPO3
SO3
Orgnic acid
Protein
27
103
1
0.5
6
0.8
Total 151 Total 138.3
Plasma Osmotic Pressure
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Relation between Osmotic pressure
and distribution of body fluid
Osmotic Pressure
Crystal OP and Colloid OP
Plasma Crystal OP :
[Na+] contributes to a major portion of
OP
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Plasmatic Colloid OP
Plasma protein contributes a forceleading to distribution of ECF
Interstitial Crystal OP
Contributes to the shift of extracellular
and intracellular water
Relation between Osmotic pressure
and distribution of body fluid
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Plasma
Interstitial Fluid
ICF
EC
F
Colloid OP Plasmatic protein
Crystal OP
Semi-permeable membrane
Crystal OPColloid OP
Crystal OP
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The Regulation of
Body Fluid Balance
Maintaining normal osmotic pressure
Maintaining normal concentration &
Integral dose of natrium
Maintaining normal Volume (Blood-volume)
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posterior
hypophysis
A D H
Distal renal
tubules
& collecting
tubules
Sensitivity ECF Osmotic pressure 1 2
6 mOsm Release of ADH
Maintaining osmotic pressure
hypothalamus
osmotic pressure
receptor
The Regulation of
Body Fluid Balance
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Maintaining the concentration & Integraldose of natrium
Distarenal
tuble
macular
densa
adrenalortex
renin angiotonin
aldosterone Increased Na reabsorption &
eliminating K Decreased removing HCO3-
acid urine
The Regulation of
Body Fluid Balance
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Volume regulation (Blood-volume)
Glomerulus
paracell+adrenal cortex
aldosterone
renin
angiotonin
Assaying CVPAP& PAWP
The Regulation of
Body Fluid Balance
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Classification of body
fluid change ( Four Types )
Volume Changes(ECF)
Volume Deficit
Volume Excess
Concentration Changes
Hyponatremia
Hypernatremia
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Mixed volume and Concentration
Abnormalities
ECF Deficit and Excess with Hyponatremia
ECF Deficit and Excess with Hypernatremia
Classification of body
fluid change( Four Types )
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Composition Changes
Acid-base disturbances
Potassium, Calcium, Magnesium
abnormalities
Classification of body
fluid change( Four Types )
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Isotonic ECF deficit
(Na+=135-145mmol/l )
Volume Changes
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Etiologies ( Acute )
External-losses:
gastrointestinal fluids due to vomiting,nasogastric suction, diarrhea, and
digestive tract fistula
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Internal-losses : sequestration (Third Space
Soft tissue injuries and infection, burns
Intra-abdominal and retroperitoneal
inflammation
intestinal obstruction, bowel wall, peritonitis
Etiologies ( Acute )
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Clinical Manifestations
Moderate Serve
CNS Sleepiness, apathy, slow
responses, anorexia
Cessation of usual
activity
Decrease tendon reflexes
Anesthesia of distal
extremities Stupor
Coma
GI Progressive decrease in
food consumption
Nausea, Vomiting
Refusal to eat
Silent ileus and distention
CV Orthostatic hypotension
Tachycardia
Collapsed veins
Collapsing pulse
Cutaneous lividity
Hypotension
Distant heart sounds
Cold extremities
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moderate serve
Tissue signs Soft,small tongue
longitudinal wrinkling
Decreased skin
Atonic muscles
Sunken eyes
Metabolism Temperature Temperature
Clinical Manifestations
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Diagnosis
Etiology
Clinical manifestation : Seeing Table
Laboratory
Increased RBC,WBC,PLT and plasmaprotein
Increased HCT
Normal serum sodium & chloride
hyperbaric urine
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Fluid & electrolyte therapy
To eliminate etiologies
Quality of Solution
Isotonic sodium solution
Lactated Ringers solution Quantity
hydropenic quantity+continuous losses
quantity+physiological quantity Rate and Goal
To moderate BP & Pulse rate
Urinary Output 30 50 ml / hr
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Isotonic ECF excess
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Etiology
Iatrogenic
Secondary to renal insufficiency
Major
operation
Severe trauma
Infection
Renal vascular constriction
Increased ADH & Aldosterone
Retention of
sodium & water
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Clinical manifestations
Circulatory overload
Basilar rales
Heart failure
Tissue signs
Subcutaneous pitting edema
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Fluid & electrolyte therapy
Restriction of water & sodium
Colloid + Diuretics
Hypertonic diuresis:
relieve cerebro-edema 20% mannitol
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Mixed volume and Concentration
Abnormalities
Hypotonic ECF deficit
(Na+
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Etiologies (Secondary)
Continues to drink water while losing large
volumes of gastrointestinal fluids.
The loss of a large amount of salt, such asvia sweat, and kidney.
In the postoperative period when
gastrointestinal losses are replaced withonly hypotonic sodium solution.
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Clinical manifestations
CNS signs increased intracranial pressure
& secondary hypertension
Tissue signs excessive intracellular water
Digestive system: Vomiting, Nausea
Shock:Progressing to oliguric renal failure
promptly
Asymptomatic Untill the serum sodium
falls below 120 mmol/L
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One important exception
Closed head injury, in which mild
hyponatremia may be extremely
deleterious
Clinical manifestations
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Diagnosis
Etiology
Laboratory
Serum sodium concentration < 135mmol/L
Decreased urinary sodium and
Hypobaric urine < 1.010 Increased HCT and serum BUN & NPN
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Clinical Manifestation
Clinic
manifestation
Serum sodium
(mmol/L)
NaCl deficit
( g/kg )
Mild Symptomless 131~135 0.5
Moderate Increased ICP
(compensated)
130~121 0.5~0.75
Severe Increased ICP
(decompensated)
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Mild or moderate hyponatremia
Fluid & electrolyte therapy
Eliminating etiologies
Quality of solution: NS 5%GNS and or5%NaCl
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Severe hyponatremia
Fluid & electrolyte therapy
TBW (liters) =Body weight ( kg ) 0.6 (female 0.5)
Sodium deficit (mmol)= Serum sodium (standard
actual) TBW
Total Amount:Half of sodium deficit + Requisite
amount per day
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Quality:
5%sodium chloride solution (2/3) +
Isotonic sodium chloride (1/3)
Shock
colloid: crystalloid=1:2~3
Convulsions or coma
5%NaCl 100 ~ 250 ml
Severe hyponatremia
Fluid & electrolyte therapy
S h t i
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Rate of increment of sodium
is 0.5~1mmol/L/h; and no more than 12
mmol/L within 24hs
Complication:
Osmotic Demyelination Syndrome(ODS).Pontine demyelination
Severe hyponatremia
Fluid & electrolyte therapy
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Management of severe acute and
chronic hyponatremia
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EFW: electrolytefree water
Th f S A
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Therapy for Severe Acute
hyponatremia
Aim:
Shrink the size of brain cells with hypertonic saline
Na+
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How to calculate the amount of 10 NaCl
per hour
Raising [Na + /h] Kg 0.6( 0.5)= the
amount of mmol of NaCl
Therapy for Severe Acute
hyponatremia
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W t i t i ti
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Water intoxication
(Dilutus hyponatremia)
Retention of water in the body
[Na+] is decreased
Intracranial pressure is increased highly Management
Stopping infusion of water
Diuresis
Negative balance of water
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Hypertonic ECF deficit
(Na+>150 mmol/l )
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Etiology(Primary)
Restricted water intake in circumstances:
Sweat
Burn
Diabetic coma
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Clinical manifestations
Central nerve system
restless,weakness,delirium,maniacal
behevior, coma Tissue signs -dry and thirsty, sticky mucous
membranes
Dehydration fever Tachycardia
Oliguria
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Diagnosis
Etiology
Laboratory
Increased sodium ( >150mmol/L) & HCT
Hyperbaric urine
Clinical Manifestation
Extremely thirsty
High fever
Oliguria
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Fluid & electrolyte therapy
Principles
-Adopting 5 GS , 0.45% NaCl , water viaintestine
-Half of volume deficit Requisite amountper day
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Measures
with loss 1% body weight infusing
400 500ml
supplemental quantities (ml)
= [actual serum sodium normal serum
sodium (mmol/L)] body weight (kg) 4
Fluid & electrolyte therapy
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Classification of ECF changes
ECF deficit ECF excess
Isotonic normal Na+
normal Na+
hypotonic hyponatrium hyponatrium
hypertonic hypernatrium hypernatrium
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Composition Changes
Hypokelamia(
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Common cause
Excessive excretion:
Kidney ; Digestive tract (Vomiting, Diarrhea,
Gastric suction, Intestinal fistula)
Less in-take:
Less dietary intake ; potassium-free parenteral
fluids
RedistributionThe transfer of extracellular potassium into cells
Alkalosis
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2Na+
1H+ 3K+
Cell
H++HCO3- =H2O+CO2
2Na
+
1H+3K+
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Clinical manifestations
General:
Anorexia,Nausea,Vomiting
Skeletal muscles
(Diminished to absent tendon reflexes,
respiratory hypoventilation)
Smooth muscles(Paralytic ileus )
Cardiac muscles (Hypotension)
Muscular weakness
Flaccid paralysis ( k + < 2.5mmol / L
Clinical manifestations
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CNS Serum potassium 2.0mmol/L MorbusObnubilation disorientation
Cardiovascular
ECG: ST segment depression,
decreased T wave, Increased U wave,
T < U
Arrhythmia: Premature ventricular and aterial contractions
ventricular and aterial tachyarrhythmias
Clinical manifestations
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Diagnosis
History
Clinical symptoms
Serum potassium 3.5 mmol/L
EKG
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Treatment
The quantities of supplemental potassium
Serum potassium 3mmol/L. To replace
200 400mmol May be increased by
1mmol/L Serum potassium 3 3.5mmol/L
To replace 100 200mmol May be
increased by 1mmol/L
The rate of administration (intravenous)
Should not exceed 20 mmol K+ / hr
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Attention
Therapy of shock
Urine output arrive at 40 ml/hr, and
potassium infused
No more than 40 mmol K+added to 1 liter
(0.03%) of IV fluids via peripheral vein
infused
Calcium not infused
Treatment
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Hyperkelamia(>5.5mmol/L)
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Common causes
Excessive potassium entered into blood
circulation Iatrogenicity , Infusion of excessive potassium
Infusion of a vast reserve of blood
Renal excretion decreased
Abnormal distribution
Acidosis Acute tumor lysis, burn, Acute intravascular
hemolysis
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Clinical manifestations
GastrointestinalNausea & vomiting
Intermittent colic & diarrhea
Paresthesia & Weakness Cardiovascular
Bradycardia
Microcirculatory dysfunction ( Be cold, cyanosis, pale and hypotension)
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Clinical manifestations
EKG
Shortening of QT interval and high peaked T
wave
Widened QRS , PR interval prolongation
disappearance of P wave
degeneration of the QRS to a sine wave
pattern
Ventricular asystole or fibrillation
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Diagnosis
Any inexplicable symptoms
ECG
Serum potassium ion > 5.5mmol/L
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Lowering of serum potassium
Transfer potassium into cells 5%
NaHCO3;11.2% Sodium lactate, GI
Diuretics
Cation-exchange resins (oral ;
maintaining clysis)
Peritoneal dialysis, or hemodialysis,
hemofiltration
Treatment
Hyperkelamia
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Hyperkelamia
EKG change
Effect in 10min
calcium
gluconate V.Removeccause
Aversilon intra-
cell Insulin
NaHCO3
Urinary
systerm
urinepotassium
gastroin
testinal
Decrease oral
ion exchange resin,coloclysis
low
hemodialysis
Increase egest:
Mineralocorticoid
NaHCO3
Acetazolamide
yes no
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Disturbances of Calcium
Hypocalcemia(
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Hypocalcemia
Causes: acute pancreatitis; renal failure; intestinal fistula;
Infusion of a vast reserve of blood; blood purification
ManifestationSymptoms:numbness; tingling;Apnea; Tetany
Signs: Hyperactive tendon reflexes; Chvosteks Signs
Treatments:10%calcium gluconate;5%Calcium Chloride
H l i ( 4 0 l/L)
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Hypercalcemia(>4.0mmol/L)
Causes:
hyperparathyroidism;
Bony Metastasis
Manifestations:
Fatigue; Vomiting
Treatment:
EDTA; Na2SO4; Calcitonin
Magnesium
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Magnesium
deficiency(
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Hypophosphatemia
(
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Acid-base imbalance
Buffer systemA weak acid or base & the salt of that acid or base
Intracellular Extracellular Red cell
B.Protein/H.Protein B.HCO3/H2CO3 B.Hb/HHb
B2HPO4/ BH2PO4 B.HbO2/HHbO2
Anion Gap=[Na+] [Cl-+HCO3-]
Th i t t l f t i
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The important role of potassium
Assumption:
pre- existing potassium depletion
Outcome:
Intracellular (3 K )and extracellular
( 2Na+ 1 H+ ) exchange
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Decreased Na+ and K+ exchange, Increased
H+ and Na+ exchange in renal tubule
Paradoxical acid urine
Metabolic alkalosis is aggravated
The important role of potassium
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The important role of the lung
Sensible acids are excreted via the lung
HCI NaHCO3 NaCI H2CO3
H2O CO2
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The important role of the kidney
Insensible acids excreted by kidney
Inorganic acid anions hydrochloric sulfuric
hosphoric acids with hydrogen H+ Na+ exchange
ammonium salts H+ NH3NH4-
organic acid anions lactic keto
pyruvic acids Be metabolized
Some renal excretion with high levels
H d H lb l h i
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Henderson - Hasselbalch equation
BHCO3-
pH pK log
H2CO3
27mmol/L6.1 log
1.35mmol/L
2 0
6.1 log1
6.1 1.3 = 7.4
B h
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Bohr
H
HbO2+H++CO2 Hb +O2
CO2
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normal
Shift right
Shife lefe
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Metabolic Acidosis(pH
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Metabolic Acidosis(pH
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Clinical manifestations
Increased in depth & frequency ofrespiration (Kussmaul breathing)
Peripheral vessels dilated Circulatory
shock, Cerise lip
Decreased muscular tension & tendon reflex
merged
Unconsciousness
Treatments
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Treatments
Principles
Therapy for basic disease
Alkali treatment: dose initials 1 / 3 ~ 1 / 2 requisite
amount
Pre-treatment: serum K+ & Ca++
Treatments
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The amount of Alkali necessary
normal CO2-CP - serum CO2-CP
TBW Kg BE 3 BW Kg
normal SB observed SB BW
Kg Loss of base mEq
Treatments
Treatments
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Some of alkalescent solution contains HCO 3
1 gm NaHCO3 12 mmol HCO3 -
1ml - 11.2%NaC3H5O3 1 mmol HCO3 -
1ml - 3.63%THAM 0.3 mmol HCO3 -
Treatments
Respiratory Acidosis(pH
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Respiratory Acidosis(pH
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Clinical manifestation
Advanced respiratory insufficiency(Apnea)
Metabolic encephalopathy (headache,drowsiness, stupor and coma, papilledema)
Blood pressure elevated reduced
Ventricular fibrillation (hyperkalemia)
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Treatment
Treatment of Causes
To improve ventilation
Alkalescent solution is harmful !!
Metabolic alkalosis(pH>7 45)
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Metabolic alkalosis(pH>7.45)
Defects Causes Compensation BHCO3/H2CO3
Loss of fix vomiting or gastric Pulmonary (rapid) >20/1
Acids suction with decreased rate (numerate
pyloric obstruction & depth of breath into increase)
Gain of base excessive intake of Renal (slow)
Bicarbonate bicarbonate excretion
bicarbonate
Potassium, Diuretics retention of acidChloride of salts, decreased
Depletion ammonia formation
Clinical manifestations
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Clinical manifestations
Peripheral vessel constricted
Mental symptoms: Delirium, Drowsiness
Decreased in depth & frequency ofrespiration
Tetany & tendon reflex accentuation
Treatment
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Treatment
Therapy for basic disease
Correction of the underlying disturbances
Loss of gastric fluid replaced with NS or GNS potassium deficit correction of hypokalemia
Serum HCO3 ,45 50 mmol/L pH>7.65
0.1 M hydrochloric acid solution IV
Treatment
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Hydrochloric acid mmol
[actual serum HCO3-- normal serum HCO 3 -
mmol/L ] BW kg 0.4
[normal plasma CI - actual plasma CI mmol ]BW kg 0.2 0.6
The initial dose of hydrochloric acid:
1 / 2 dose of above mentioned
Treatment
Respiratory alkalosis(pH>7 45)
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Respiratory alkalosis(pH>7.45)
Defects Causes Compensation BHCO3/H2CO3
Excessive Hyperventilation Renal >20/1
Loss of Apprehension,Hypomia Excretion of (denominator
CO2 severe pain, high bicarbonate, decreased)
Increased temperature,assisted acid salts
Alveolar ventilation,encephalitis Decreased
Ventilation ammonia formation
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Treatment
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Treatment
Therapy for basic disease
Increase pulmonary dead space
5% CO2 added to the inspired air
Dangerous!!!
How to differentiate the four types of
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acid-base imbalance
Arterial blood gases test
AB: actual bicarbonate(Both metabolismand respiration)
SB: Standard bicarbonate(Only metabolism)
SB 38 760mmHg PCO2 40mmHg fullyoxygenated Hb
BE: Base excess
The four types of
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acid-base disturbances
AB = SB = Normal Normal
AB = SB < Normal Metabolic acidosis
AB = SB > Normal Metabolic alkalosis
AB > SB Respiratory acidosis
AB < SB Respiratory alkalosis
Case Studies
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Case Studies
1 Found Down
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1. Found Down
45 yo WM, found down, presumed to beassaulted, well known to ED for EtOH
CT head - hygromas, small ICH
labs:Na = 118
K = 2.4
Cl = 74
What do you think? What do you do?
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Severe Hyponatremia
Severe Hypokelamia Management
Correct sodium to above 120 mEq/dl
NaCl + 40 mEq/L KCl
3% Saline furosemide diuresis (euvolemic)
serial electrolytes
be prepared to handle seizures
Replace potassium Cl should correct itself
2 JO
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2. JO
JO is a 58 year-old male with cirrhosis ofthe 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 hishyponatremia?
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JOs is in an edematous state. He has anexcess of TB water and sodium. The
appropriate treatment is water and sodium
restriction. He should also receive diuretictreatment. The drug of choice is Aldactone
(spironolactone), an aldosterone antagonist.
3. Mrs Jones
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3. Mrs Jones
Mrs Jones. is a 62 year-old female who is having anacute exacerbation of Crohns disease. Shecomplains to you of severe and frequent diarrheaover the last four days. She experiences dizzinesswhen she stands. Your physical examination
reveals dry mucous membranes. In the supineposition her BP=110/65 and in the upright positionher BP=90/45 and her pulse=140. Your lab valuesare as follows:
Na 132, K 2.9, Cl 92, CO231, BUN 25, Cr 1.0
Discuss Mrs. Ds fluid and electrolyte problems.
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Mrs Jones has extracellular volume depletion due toprolonged diarrhea. The ECVD is supported by herphysical assessment and postural hypotension and herBUN/Cr is > 20:1. The diarrhea has resulted in a loss offluid and sodium chloride. Some potassium was lostdirectly in the stools, but the main cause of her
hypokalemia is her ECVD which has induced a metabolicalkalosis (contraction alkalosis.) The alkalosis contributedto her hypokalemia by two mechanisms. Some potassiumhas moved to the intracellular compartment but much of ithas been lost in the urine where potassium wasting occurs
secondary to chloride deficit. Administration of NormalSaline with Potassium Chloride will correct her fluid andelectrolyte problems (and alkalosis.)
4. M.T.
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4. M.T.
M.T. is a 55 year-old female with a history of chronic renalfailure who is admitted to the SICU following a motorvehicle accident. She is started on a TPN solution withminimal K, no Mg and no Phos. She also receivesMylanta II 30 ml per NG tube every four hours.Although her baseline labs were normal on day six herlabs are as follows:
K 4.3, Mg 2.6, Phos 1.6
1. What role did the antacid play in her electrolyteabnormalities?
2. What role did the TPN play?
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M.Ts K is normal, but she has hypermagnesemiaand hypophosphatemia. The antacid contributed
to both of these abnormalities. It provided asignificant source of Mg this patient with impairedexcretion. Also the aluminum in the antacid acteda phosphate binder contributing to thehypophosphatemia.
The TPN could have contributed to thehypophosphatemia by inducing an intracellularshift of phosphate (refeeding.) The potassium
probably remained normal because some wasbeing provided. Mg was being provided enterally.
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