Gangguan Pada Keseimbangan Elektrolit

8/18/2019 Gangguan Pada Keseimbangan Elektrolit

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GANGGUAN PADA KESEIMBANGANELEKTROLIT

dr. Andi Sulistyo Hariboo! S".PD.

SPESIALIS PEN#AKIT DALAM

Pro$ra% Studi P&ndidi'an Do't&r

UNI(ERSITAS ISLAM MALANG

)*+)


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FLUIDS and ELECTROLYTES

ELECTROLYTES

Functions of Electrolytes

Contribute most of the osmotically active

particles in body fluids

Provide buffer systems for pH reulation

Provide the proper ionic environment fornormal neuromuscular irritability ! tissuefunction


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DISTRIBUTION O, ELE-TROL#TES


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-ATIONS AND ANIONS IN BOD# ,LUIDS

Figure 27.2


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DISTRIBUTION O, MAORELE-TROL#TES• Na+ and CL- predominate in extracellular fluids

(interstitial fluid and plasma) but are ver lo!

in t"e intracellular fluid (ctoplasm)

• #+ and $%&'2- predominate in intracellular fluid

(ctoplasm) but are in ver lo! concentration in

t"e extracellular fluids (interstitial fluid and

plasma)

• t bod fluid p$ proteins *%- act as anions,

total protein concentration *%- is relativel

"ig" t"e second most important anion in t"e

ctoplasm *%- is intermediate in blood plasma

but *%- is ver lo! in t"e interstitial fluid


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DISTRIBUTION O, MINORELE-TROL#TES• $C&/- is in intermediate concentrations in all

fluids a bit lo!er in t"e intracellular fluid

(ctoplasm), it is an important p$ buffer in t"e

extracellular comparments

• Ca++ is in lo! concentration in all fluid

compartments but it must be tig"tl

regulated as small s"ifts in Ca++ concentration

in an compartment "ave serious effects

• 0g++ is in lo! concentration in all fluid

compartments but 0g++ is a bit "ig"er in t"e

intracellular fluid (ctoplasm) !"ere it is a

component of man cellular en1mes


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REGULATION O, ELE-TROL#TES 0aor Cations in bod fluids

3odium (Na+)

%otassium (#+)

Calcium (Ca++)0agnesium (0g++)


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PRIN-IPLES O, ELE-TROL#TEDISTURBAN-ES


4mplies an underling disease process

5reat t"e electrolte c"ange but see6 t"ecause

Clinical manifestations usuall not specific to

a particular electrolte c"ange e.g.

sei1ures arr"t"mias

4mplies an underling disease process

5reat t"e electrolte c"ange but see6 t"ecause

Clinical manifestations usuall not specific to

a particular electrolte c"ange e.g.

sei1ures arr"t"mias


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Clinical manifestations determine urgency

of treatment, not laboratory values Speed and magnitude of correction

dependent

on clinical circumstances

Frequent reassessment of electrolytes

required

Clinical manifestations determine urgency

of treatment, not laboratory values Speed and magnitude of correction

dependent

on clinical circumstances

Frequent reassessment of electrolytes

required


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ELE-TROL#TES / THEIR IMBALAN-ES

SODIUM 0NA12

Sodiu% balan3&

Sodiu% 4 %a5or 3ation in &6tra3&llular 7luid 0E-,2

Sodiu% 4 %ost 3o%%on "robl&% it8 &l&3trolyt& balan3&

K&y to balan3&9 in$&stion :ia G;I tra3t 4 &63r&tion :ia 'idn&y Aldost&ron& 3ontrols sodiu% l&:&ls :ia t8& 'idn&y

R&%&%b&r aldost&ron&


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DISORDERS O, SODIUMBALAN-ENa+ is t"e most abundant electrolte in t"e

CF.

Na+ and accompaning anion Cl- areresponsible for normal osmotic activit of t"e

CF.

ll gain8loss of Na+ is accompanied b

gain8loss of !ater.


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H#PONATREMIA $povolemic "ponatremia

• 9omiting

• :iarr"ea

• :iuretics

• drenal insufficienc Normovolemic "ponatremia

• 3ndrome of inappropriate secretion of antidiuretic "ormone

• ;enal failure

•


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-LINI-AL MANI,ESTATIONS O,H#PONATREMIA Neurologic

• 3ei1ure

• Coma

• gitation

=astrointestinal

• norexia

• Nausea8vomiting

0uscular

• Cramps

• !ea6ness

• $eadac"e

• Cerebral edema

• Confusion


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TREATMENT O, H#PONATREMIA Fluid restriction

dministration of "pertonic saline and an

osmotic or loop diuretic

>>>Correction of serum sodium levels too

rapidl can result in neurologic damage and

central pontine melinolsis>>>


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H#PONATREMIA cute smptomatic "ponatremia

Correct no faster t"an ? m@8L per "our for t"e

first A-B m@8L

No more t"an ?-?2 m@8L in first 2' "ours

DE saline is almost never needed

Calculate t"e Na deficit Na m@ (*Na desired - *Na measured) G 5H< 5H< .D or .A G !eig"t in #=


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-AUSES O, H#PERNATREMIA 0ost common cause is !ater deficienc d8tI

• xcessive loss

• 4nade@uate inta6e

lso ma be caused bI

• xogenous Na+ load

• %rimar "peraldosteronism

• :iabetes insipidus• ;enal dsfunction


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-LINI-AL MANI,ESTATIONS O,H#PERNATREMIA

5remulousness

4rritabilit

taxia

0ental confusion

Coma d8t cerebral !ater loss


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TREATMENT O,H#PERNATREMIA

;enal tubular diuretics

$emodialsis

5reat central diabetes insipidus !it"

vasopressin

>>>Correction of serum sodium level too

rapidl can result in neurologic damage

secondar to cerebral edema>>>


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H#PERNATREMIA 5reatment

Severe ECFV depletion is the priority and should

be corrected with NS first. 3ubse@uent fluid

replacement can be "potonic

0aor complication of overl rapid correction is

cerebral edema

3afe rate is no more t"an .D- ? m@8L per "our

3"ould ta6e /A-72 to "ours to completel correct


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H#PERNATREMIA 5reatment

Calculate t"e !ater deficit

$2& deficit 5H< G (*Na meas- *Na des)8*Na

des 4mportant to ta6e into account ongoing losses

insensible losses .D - ? liter82' "ours !it" fever t"ese losses increase b A-Bml82' "rs for

eac" degree Faren"eit


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POTASSIUM REGULATION

0aor electrolte and principle cation in t"e

extracellular fluid;egulates metabolic activities

;e@uired for glcogen deposits in t"e liver ands6eletal muscle

;e@uired for transmission of nerve impulses normal

cardiac conduction and normal smoot" and s6eletal

muscle contraction;egulated b dietar inta6e and renal excretion


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POTASSIUM 0K 12

Potassiu% balan3& Ma5or intra3&llular 3ation Balan3&9 in$&stion 4 &63r&tion 0:ia 'idn&ys2

Aldost&ron& "ri%arily 3ontrols "otassiu% It &638an$&s "otassiu% 7or sodiu%

Insulin also r&$ulat&s "otassiu% It dri:&s it into 3&lls 0it8 su$ar2 / t8us "rodu3&s

8y"o'al&%ia "H also a77&3ts "otassiu% s&3r&tionA3idosis9 %or& H1 in blood 8i38 7inds its ay into 3&ll

/ "us8&s K 1

into blood Also $&t 'idn&y to &638an$& H1 7or K 1

A3idosis ;$i:&s; 8y"&r'al&%iaAl'alosis9 l&ss H1 in blood

Kidn&ys &638an$& K 1 7or H1> t8us $&t 8y"o'al&%ia


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5"e relation bet!een potassium and "drogen ions in t"e plasma

3aladinJs natom K %"siolog fourt" edition 0c=ra! $ill


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%otassium balance in t"e bod

Costan1o %"siolog second edition 3aunders

POTASSIUM ION REGULATION IN


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POTASSIUM ION REGULATION INE-,

27-/


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H#POKALEMIACauses

• =astrointestinal losses

• 3stemic al6alosis

•

:iabetic 6etoacidosis• :iuretic t"erap

• 3mpat"etic nervous sstem stimulation

• dministration of beta-adrenergic receptor

agonists


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H#POKALEMIA 3purious "po6alemia

0ar6ed leu6octosis

dose of insulin rig"t before t"e blood dra!

;edistribution "po6alemial6alosis (# decreases ./ for ever .? increase in

p$)

4ncreased Heta2 adrenergic activit

5"eop"lline toxicitFamilial


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H#POKALEMIA xtrarenal depletion

diarr"ea

laxative abuse

s!eat losses fasting or inade@uate inta6e


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H#POKALEMIA ;enal potassium depletion

urine potassium 2 m@82' "rs

spot urine !it" 2 m@ #8gram creatinine

classified !"et"er t"e occur !it" a metabolical6alosis vomiting8N= suction diuretic tx 0ineralocorticoid excess sndromes


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H#POKALEMIA ;enal losses

metabolic acidosis ;5 5pe 4 and 44 :# Carbonic an"drase in"ibitor t"erap Mreterosigmoidostom

No acid-base disorder 0g deficienc

:rugs


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-LINI-AL MANI,ESTATIONS O,H#POKALEMIA utonomic neuropat"

36eletal muscle !ea6ness

4ncreased sensitivit to :igoxin

Cardiac

• :ecreased mocardial contractilit

• lectrical conduction abnormalities• rr"t"mias

• 5ac"cardia

• 9entricular fibrillation


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POTASSIUM

Copyright 2008 by Pearson Education, Inc.


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H#POKALEMIA AND THE EKG• %rolonged %; interval

• %rolonged 5 interval

•


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TREATMENT O, H#POKALEMIA 3lo! 49 potassium supplements

nest"esia related concernsI

• 4ncreased ris6 of mocardial irritabilit #+ O2.A• void "perventilation of t"e lungs

• void glucose containing 49 solutions

• void rapid infusion of 49 #+ supplements


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H#PERKALEMIA 3evere "per6alemia is a medical emergenc

Neuromuscular signs (!ea6ness ascending

paralsis respirator failure)

%rogressive C= c"anges (pea6ed 5 !avesflattened % !aves prolonged %; interval

idioventricular r"t"m and !idened ;3

complex sine !ave pattern 9 fib)


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H#PERKALEMIACauses

• 4ncreased total bod potassium

• ;enal failure

• %otassium-sparing diuretics

• xcessive 49 #+ supplements

• xcessive use of salt substitutes

• ltered distribution of potassium

• 0etabolic or respirator acidosis

• :igitalis intoxication• 4nsulin deficienc

• $emolsis

• 5issue and muscle damage after burns

• dministration on succinlc"oline


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-LINI-AL MANI,ESTATIONS O,H#PERKALEMIA

reflexia


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H#PERKALEMIA AND THE EKG• Narro!ing and pea6ing of 5 !aves

• ?st degree 9 bloc6

• ;3 !idening

• 35 segment depression

• %rogression to merging of ;3 an

5 !aves to a sine !ave

• 5ac"cardia

• 9entricular fibrillation


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H#PERKALEMIAH#PERKALEMIA

tiolog P renal failure

transcellular s"ifts cell

deat" drugspseudo"per6alemia

0anifestations P

cardiac neuromuscular

tiolog P renal failure

transcellular s"ifts cell

deat" drugspseudo"per6alemia

0anifestations P

cardiac neuromuscular


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TREATMENT O, H#PERKALEMIA%rimar goal

void adverse cardiac effects 4nsulin and glucose to s"ift #+ into cells 49 calcium to antagoni1e cardiac effects of

"per6alemia

nest"esia related concernsI serum #+ of D.Dm@8L is upper limit for elective

procedures


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H#PERKALEMIA 5reatment

3top potassium>

=et and C=

Hyperkalemia with ECG changes is a medical

emergency


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First p"ase is emergenc treatment to

counteract t"e effects of "per6alemia 49 Calcium

5empori1ing treatment to drive t"e potassium

into t"e cells glucose plus insulin

Heta2 agonist

Na$C&/


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5"erap directed at actual removal of potassium

from t"e bod sodium polstrene sulfonate (#aexalate) dialsis

:etermine and correct t"e underling cause


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-AL-IUM 0-A112

-al3iu% balan3& -al3iu% is %ost abundant %in&ral in body

-al3iu% is i%"ortant as an &6tra3&llular 3ation

-al3iu% / "8os"8orus 8a:& a r&3i"ro3al r&lations8i"

-al3iu% balan3& is d&"&nd&nt on9

Parat8yroid 8or%on& 0PTH2

-al3itriol 0a3ti:& :ita%in D2

-al3itonin 07ro% t8yroid2

?@ o7 3al3iu% r&absorb&d at t8& 'idn&ys

-al3iu% 7un3tions Stru3tural str&n$t8 7or bon&s / t&&t8

Maintains stability o7 n&r:& %&%bran&

R&uir&d 7or %us3l& 3&ll 3ontra3tion

N&3&ssary 7or blood 3lottin$


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REGULATION O, -AL-IUM IONS

;egulated !it"innarro! rangelevated extracellular

levels prevent

membranedepolari1ation:ecreased levels lead

to spontaneous actionpotential generation

5erms$pocalcemia$percalcemia

%5$ increases Ca2+

extracellular levels

and decreases

extracellular

p"osp"ate levels 9itamin : stimulates

Ca2+ upta6e in

intestines

Calcitonin decreases

extracellular Ca2+

levels

27-D


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REGULATION O, -AL-IUM IONS

27-D?


52/79

H#PO-AL-EMIACausesI

• :ecreased serum albumin concentration

• C"elation of calcium b citrate

• ;"abdomolsis

• $poparat"roidism

• %ancreatitis

• ;enal failure


53/79

-LINI-AL MANI,ESTATIONS O,H#PO-AL-EMIA

Neuromuscular irritabilit• 5etan

• Larngospasm

•

$peractive deep tendon reflexes


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TREATMENT O, H#PO-AL-EMIACalcium replacement

4ntraoperative P "perventilation and

respirator al6alosis


55/79

H#PER-AL-EMIACausesI

• Calcium mobili1ation from bone due to

immobilit

• 5umors

• $perparat"roidism


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-LINI-AL MANI,ESTATIONS O,H#PER-AL-EMIA

norexia

Nausea

Constipation

Cognitive depression#= c"anges

• %rolonged %; interval

• 3"ortened 5 interval

• %9CJs

TREATMENT O,


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TREATMENT O,H#PER-AL-EMIA5reatment of underling cause

9olume expansion

4ntraoperative "percalcemia s"ould be

managed !it" administration of ade@uatefluids and maintenance of urine output.


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Copyright 2008 by Pearson Education, Inc.


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REGULATION O, -HLORIDE /MAGNESIUM IONS C"loride ions%redominant anions in CF

0agnesium ions

Capacit of 6idne to reabsorb is limitedxcess lost in urine:ecreased extracellular magnesium results in

greater degree of reabsorption

27-DQ


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MAGNESIUM REGULATION ssential for en1me activities Neuroc"emical activities

Cardiac and s6eletal muscle excitabilit

;egulation :ietar

;enal mec"anisms

%arat"roid "ormone action

D P AE of magnesium contained in bones ?E in CF

0inimal amount in cell

REGULATION O, BLOOD


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REGULATION O, BLOODMAGNESIUM

27-A?


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H#POMAGNESEMIA 3erum magnesium less t"an ?.Dm@8L

CausesI• 4nade@uate inta6e of magnesium

• 5%N

• =astrointestinal losses

• %ancreatitis

• %arat"roid "ormone disorders

• $peraldosteronism

• #etoacidosis• C"ronic alco"olism


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-LINI-AL MANI,ESTATIONS O,H#POMAGNESEMIA

CN3 irritabilit• 3ei1ures

•

$perreflexia

• 36eletal muscle spasm

TREATMENT O,


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TREATMENT O,H#POMAGNESEMIA

49 administration of magnesium sulfate


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H#PERMAGNESEMIA 3erum magnesium level greater t"an 2.D

m@8L

CausesI• 4atrogenic administration

• %reeclampsia

• ntacids8laxatives

• ;enal failure


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-LINI-AL MANI,ESTATIONS O,H#PERMAGNESEMIA

CN3 depression stupor coma

36eletal muscle !ea6ness respirator failure

:ecreased perip"eral vascular tone

:ecreased mocardial contractilit

5ocolsis

H#PERMAGNESEMIA AND THE


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H#PERMAGNESEMIA AND THEEKG%rolonged % interval


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TREATMENT O,H#PERMAGNESEMIA 3upportive care

Fluid loading

:iuresis

cute "permagnesemia P49 calcium to

counter t"e elevated magnesium levels


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ANIONS -ONT


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PHOSPHATE

27-7


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OTHER ELE-TROL#TE DE,I-ITS-A! POC! MG

OTHER ELE-TROL#TE DE,I-ITS-A! POC! MG

0a produce serious but nonspecific cardiac

neuromuscular respirator and ot"er effects

ll are primaril intracellular ions so deficits

difficult to estimate

5itrate replacement against clinical findings

0a produce serious but nonspecific cardiac

neuromuscular respirator and ot"er effects

ll are primaril intracellular ions so deficits

difficult to estimate

5itrate replacement against clinical findings


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PHOSPHATE

4nvolved in acidPbase buffering sstem 5%production and cellular upta6e of glucose

0aintenance re@uires ade@uate renal functioning

ssential to muscle ;HCs and nervous sstem

function


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H#PERPHOSPHATEMIA

$ig" serum %&'/−

caused bcute or c"ronic renal failure

C"emot"erap

xcessive ingestion of p"osp"ate or vitamin :

0anifestationsCalcified depositionI oints arteries s6in 6idnes

and corneas

Neuromuscular irritabilit and tetan


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H#PERPHOSPHATEMIA

0anagement 4dentif and treat underling cause

;estrict foods and fluids containing %&'/−

de@uate "dration and correction of "pocalcemic

conditions

H#POPHOSPHATEMIA


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H#POPHOSPHATEMIA

Lo! serum %&'/−

caused b0alnouris"ment8malabsorption

lco"ol !it"dra!al

Mse of p"osp"ate-binding antacids

:uring parenteral nutrition !it" inade@uate

replacement

H#POPHOSPHATEMIA


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H#POPHOSPHATEMIA

0anifestationsCN3 depression

Confusion

0uscle !ea6ness and pain

:sr"t"mias

Cardiomopat"

H#POPHOSPHATEMIA


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H#POPHOSPHATEMIA

0anagement&ral supplementation

4ngestion of foods "ig" in %&'/−

49 administration of sodium or potassium p"osp"ate


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+??


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