20336123 body fluid electrolyte management

7/30/2019 20336123 Body Fluid Electrolyte Management

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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


fluid change( Four Types )


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Composition Changes

Acid-base disturbances

Potassium, Calcium, Magnesium

abnormalities


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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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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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



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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


Eliminating etiologies

Quality of solution: NS 5%GNS and or5%NaCl


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Severe hyponatremia


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


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



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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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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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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



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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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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



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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



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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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GastrointestinalNausea & vomiting

Intermittent colic & diarrhea

Paresthesia & Weakness Cardiovascular

Bradycardia

Microcirculatory dysfunction ( Be cold, cyanosis, pale and hypotension)


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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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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



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Peripheral vessel constricted

Mental symptoms: Delirium, Drowsiness

Decreased in depth & frequency ofrespiration

Tetany & tendon reflex accentuation

Treatment


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Treatment


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


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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20336123 body fluid electrolyte management

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