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Fatya Annisa H
GangguanKeseimbangan Sirkulasi,Elektrolit dan
Asam-Basa
1
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Massa Tubuh Total
Perempuan Laki-laki
45%
Solids
40%
Solids
55%
Fluids
60%
Fluids
2! "#F
1! $#F
"#F "ntra &ellular 'luid #"S &airan
intra selular $#F e(tra &ellular 'luid #$S &airan
ekstra selular
)5-*0%
20-25%
#airan
interstisi
alPlasma
2
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+ompartemen #airan
Fi,ure 2)1b The #omposition o' the .uman /od
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Fi,ure 2)1a The #omposition o' the .uman /od
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Perpindahan #airan $lektrolit
3i'usi
• perpindahan molekul dari tekanankonsentrasi tin,,i ketekanankonsentrasi rendah
smosis
• perpindahan air dari konsentrasi at terlarut rendah kekonsentrasi at terlarut tin,,iosmolaritas ukuran konsentrasi suatu larutan- isotonus → konsentrasi larutan plasma darah
Transport akti'
• perpindahan molekul dari tekanankonsentrasi rendah ke
konsentrasi tin,,i d,n men,,unakan ener,i
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7erakan #airan
Fi,ure 2)! Fluid 7ains and Losses
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9
Tekanan #airan
Tekanan osmotik
• Tekanan untuk men&e,ah aliran osmotik &airan
Tekanan onkotik
• 7aa tarik &airan koloid a,ar air tetap berada dalamplasma darah di intra8askular
Tekanan hidrostatik 9≈ filtration force:
• Tekanan an, di,unakan oleh air dalam sistem tertutup
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Tekanan #airan
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KELAINAN KESEIMBANGAN CAIRAN
11
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Perubahan ;olume dan smolaritas #airan
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3ehidrasi
7an,,uan keseimban,an air
utput < "ntake
3alam Tubuh ;olume air berkuran,=
osmolaritas menin,kat
+eadaan >
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KELAINAN SIRKULASI
1?
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.iperemi pasi'
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GANGGUAN KESEIMBANGAN ELEKTROLIT
2!
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+ompartemen #airan
Fi,ure 2)2 #ations and @nions in /od Fluids
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25
Keseimbangan Natrium
- !a"# ion utama diluar sel$ !# %&' me()*
- Intrasel %0 me()*
- +ipertahanan oleh sistim !a--/P ase- /mat menentuan osmolalitas e1trasel selain
adar gluosa dan ureum.
- hiponatrium: aibat hilangnya !a") retensi cairan
- hipernatrium: hilangnya cairan) retensi ion !a.
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+eseimban,an $lektrolit
Fi,ure 2)4 The .omeostati& Ae,ulation o' Bormal Sodium
"on #on&entrations in /od Fluids
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$le&trolte /alan&e
Fi,ure 2)5 The "nte,ration o' Fluid ;olume Ae,ulation and Sodium"on #on&entrations in /od Fluids
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2*
HiponatremiaEtiologi#
%. +eplesi olume sirulasi#/+3 nai haus retensicairan hiponatremi
2. Intae urang, dehidrasi
4. 5angguan 5injal ronis# air6 hiponatremiinsu77.adrenal diare, mual, muntah, hilangnya !amel.ginjal hipo !a
4. Sindr.Inappropriate ADH (SIADH) secr.#
Ggn.neuro: in7esi, tumor, asuler, 5B8
Obatan : lorpropamid, incristin,silo7os7.
arbamaepin, tiotisen.
In!e"si paru: BC, aspergilosis, pneumonia
#as$a bedah: idiopati, /+3 etopi, arsinoma, pemberian /+3, asopresin, ositosin
&. 3iponatremi esensial
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!0
Hipernatremia
Etiologi #
%. <luid-loss# insensibel loss =demam, I8P/, lua
baar, didaerah suhu tinggi>$ diabetes insipidus$ pemberian diureti$ ggn.hipotala mus
hipodipsi o ggn. ?smoreseptor
2. Intae !a" 6# pemberian !aCl hipertoni
!a.Bi.6 atau !aCl peroral 6, sindroma Cushing
dan hiperaldosteronism
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!1
Hipernatremia
5E:/*/
Berupa 5) neurologis# letargi, elemahan otot, edutan=t@itching>, ejang2 dan oma..
erjadi o eluarnya cairan dari sel ota +apat terjadi perdarahan ota
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!2
Hipo"a%emia
3ipoalemia# - tanpa de7isit " total tubuh
- dg.de7isit " total
anpa de7isit#
- terjadi pada /lalosis Aesp. " intrasel$ juga terjadi pada hipoalemi periodi paralysis hiperalimentasi
+engan de7isit#
- asupan " urang # anoresia aloholism
- ehilangan " 66# diare hebat, muntah, la1ati7
- el.5injal# mineraloortioid6 =hiperaldosteron primer)seunder pada sirosis, 8!, deomp.>$ diureti berlebihan, pemberian penisilin atau arbenisilin$ asidosis
tubular aut, /*, hipomagnesia
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!4
Hiper"a%emia
Etiologi #
- asupan berlebih peroral)enteral
- Perpindahan " e estrasel pada asidosis
- Pseudohiperalemia# pada pem. Penderita dg.*eositosis)trombositosis o.proses oagulasi)hemolisis.
5ejala#
- elemahan otot s)d paralisa
-Dt.menurunan ", meningatan hormon2 aldosteron,insulin, epinephrin, gluagon u) menstabilan gula darah
- :antung# aritmia)arrest$ gambaran E5# tall , A8 6,interal P 6, hilangnya P, A8 menyatu dg. dan disebut
sine-&a'e
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!5
Keseimbangan Ka%sium- &0F Ca serum teriat albumin
- ''-0F di7usabel berupa ion Ca"") omples alsium
- ebutuhan alsium 0,' g)hari- saat hamil perlu tambahan 0,' g)hari
- +iet rata-rata mengandung 0,&-%,& g dg susu 2,G g)hari
- +iabsorbsi usus halus prosimal secara di7usi pasi7 - /bs. enurun o osalat, sitrat atau 7itat$ peristalti meningat
atau de7.protein
-
/bs.nai pada pemberian it.+4 =olealsi7erol>, hormon P3- Esresi melalui urine secara 7iltrasi reabsorbsi = 99F>
melalui tub.pro1.=20-40F>, *oop 3enle =%0-%'F>$tub.distal =2-G> $ reabsorbsi ini seimbang dengan abs. !a.
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!6
Hipo"a%semia
Etiologi #
%. +e7.it.+# maanan urang lema, sindrom malabsorbsi=gastretomi, panreatitis, obat pencahar>,
ggn.metab.it.+ =it.+ de7icient AicetsH el.otosomalresesi7>, renal insu7., ggn.7gs.hati, obat anti ejang
2. 3ipoparatiroidism
4. Pseudohipoparatiroidism
&. eganasan'. 3ipo7os7atemia
5ejala
otot lemah, 7asiulasi, tremor, tetani, tanda Choste, tanda
rosseau$ gelisah, psiosis
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!)
Hiper"a%semia
Etiologi#
%. 3iperparatiroidisme, 3ipertiroid
2. etastasis aner luas
4. <ratur multiple&. ieloma multiple
'. Immobilisasi lama
. ?steoporosis
. Intosiasi it.+, Intosiasi it. /
G. Insu7isiensi adrenal9. il /lali 8yndrome# o pemberian antasid disertai pemberian
susu6 pada ulus peptium atau pemberian tiasid lama bersamait.+.
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!*
Hipo!os!atemia
Etiologi#
%. /ntasid pengiat 7os7at dosis besar
2. *ua baar yg luas berat
4. +iet rendah 7os7at
&. /lalosis respiratori
'. etoasidosis diabeti . aloholisme
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!?
Hipo!os!atemia
5E:/*/
%. erusaan eritrosit
2. 5angguan 7ungsi leuosit
4. 5angguan 7ungsi trombosit
&. 5angguan 7ingsi sara7 pusat
'. Aabdomiolisis
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40
Hiper!os!atemia
Etiologi#
• Pemberian 7os7at6 peroral)enema) enteral,
pada gagal ginjal aut)roni
• Pemberian sitostatisitolisis 7os7or
eluar edalam darah
5ejala#
• etani o peneanan adar alsium
• Pengendapan alsium pd jar.luna
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41
Hipomagnesemia
Etiologi#
%. 5gn.abs.# primer, steatorea, resesi usus,
2. /loholism roni 4. etoasidosis diabeti
&. Pemberian diureti, sindr.Barter, 8I/+3,3iperaldosteron, it.+6, hiper P3
5ejala
otot lemah, 7asiulasi, tremor, tetani, tandaChoste, tanda rosseau$ gelisah, psiosis
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42
Hipermagnesemia
Etiologi
• 5angguan ginjal ronis
• Insu7isiensi hormon ortes adrenal
5ejala
• 5angguan sara7 pusat neuromusular#
–
gangguan menelan – uadriplegi
– 5angguan bicara
– elumpuhan perna7asan
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+eseimban,an $lektrolit
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GANGGUAN KESEIMBANGAN ASAM BASA
45
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46
Keseimbangan Asam - asa
- enjaga 7ungsi organ tubuh
- +iatur oleh ginjal dan paru-paru
-nilai normal p3# ,&0 " 0,02
3" pC?2 3C?4
+ i b @ /
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+eseimban,an @sam-/asa
Sistem /u''er @sam +arbonat - /ikarbonat
+ i b @ /
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+eseimban,an @sam-/asa
Sistem /u''er
@ id / / l
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@&id/ase /alan&e
7 + i b @ b
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'0
7an,,uan +eseimban,an @sam-basa
• .C naik= .#! turun
@sidosis metabolik
• .C turun= .#! naik
@lkalosis metabolik
• .C naik= Pa#2 naik
@sidosis respiratorik
• .C turun= Pa#2 turun
@lkalosis respiratorik
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51
Asidosis etabo%i"
Etiologi
• Penambahan asam baru –
asidosis latat, etoasidosis, in7esi, prod.asam usus6,eracunan metanol,etilen gliol, salisilat
• ehilangan 3C?4 =asam biarbonat> – diare, ileus
•
5injal dan Paru-paru – asidosis tub.aut,
– egagalan produsi biarbonat
@ id i M t b lik
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@sidosis Metabolik
Fi,ure 2)1! Aesponses to Metaboli& @&idosis
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@lk l i M t b lik
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@lkalosis Metabolik
Fi,ure 2)14 Metaboli& @lkalosis
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55
Asidosis *espiratori"
?leh arena paru-paru ta mampu
mengeluaran C?2#
%. 5angguan pusat perna7asan2. Penyait otot perna7asan# 5uillain Barre
8yndrome, onsmsi obat-obatan tertentu,
iastenia 5rais4. 5angguan elastisitas sal.na7as# 7ibrosis
pulm., peny.interstisial paru, obstrusi
=asma, em7isema, bronitis, bronhiolitis>
@ id i A i t ik
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@sidosis Aespiratorik
Fi,ure 2)12a Aespirator @&id/ase Ae,ulation
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5)
A%"a%osis *espiratori":
imbul aibat hiposi atau hipotensi#
%. Penyait paru# pneumonia, asma, edema paru
2. Berada didaerah tinggi)gunung4. Penyait jantung ongesti7
&. ?bat-obatan# salisilat, teo7ilin
'. 3iperentilasi primer)sentral, perna7asan
Cheyne-8toes, perdarahan sub-arachnoid. 3iperentilasi psiogeni, sirosis, sepsis,
asidosis metaboli yg.baru teratasi
. *atihan 7isi
@lkalosis Aespiratorik
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@lkalosis Aespiratorik
Fi,ure 2)12b Aespirator @&id/ase Ae,ulation
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7an,,uan +eseimban,an @sam /asa
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7an,,uan +eseimban,an @sam /asa
Fi,ure 2)11a "ntera&tions amon, the #arboni& @&id/i&arbonate/u''er Sstem and #ompensator Me&hanisms in the Ae,ulation o'Plasma p.
H+
7an,,uan +eseimban,an @sam /asa
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7an,,uan +eseimban,an @sam-/asa
Fi,ure 2)11b "ntera&tions amon, the #arboni& @&id/i&arbonate/u''er Sstem and #ompensator Me&hanisms in the Ae,ulation o'Plasma p.
H+
7 + i b
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2
7an,,uan +eseimban,an
@sam-/asa
1 @sidosis respiratori
hipo8entilasi→ retensi #2 →.2#!↑→.C↑
2 @lkalosis respiratori
hiper8entilasi →#2 banak , hilan, →.2#! ↓ → .C↓
! @sidosis metabolik
3iare= 3M→
.#!
-
↓
→
P#2 ↑
→
.C↑
4 @lkalosis metabolik
muntah → .C ↓ →.#!-↑ →P#2 ↓
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7aalKcairan-asam-basa)iun)200 4
INTERPRETASI AGD
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&
INTERPRETASI AGD
Lihat p. darah
p. D )=!5 p. < )=45
@S"3S"S @L+@LS"S
Lihat p#2 Lihat .#!-
D 40mm., < 40 mm., D 24 mM < 24 mM
M$T@/L"+A$SP"A@TA"+A$SP"A@TA"+M$T@/L"+
TERKOMPENSASI atau
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'
TERKOMPENSASI atau
TIDAK?
Lihat p. kembali- Eika mendekati kadar normal 9)=!5-)=45:⇒ terkompensasi
- Eika belum mendekati normal ⇒ tidak terkompensasi atau terkompensasi
seba,ian ika asidosis respiratorik d,n .#!
- D 24 mM ⇒terkompensasi seba,ian
ika asidosis metabolik d,n p#2 D 40 mm., ⇒ terkompensasi seba,ian
ika alkalosis respiratorik d,n .#!
-
< 24 mM ⇒ terkompensasi seba,ian
ika alkalosis metabolik d,n p#2 < 40 mm., ⇒ terkompensasi seba,ian
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L@T".@B
p. )!2= P#2 40= .#! 1?
p. )55= P#2 20= .#! 22
p. )55= P#2 !)= .#! !0 p. )4?= P#2 !5= .#! 2?
p. )!0= P#2 50= .#! 2?
p. )4!= P#2 5!= .#! !0 p. )44= P#2 !*= .#! 26
p. )4!= P#2 !2= .#! 20
@sidosis metabolik
tdk terkompensasi
@lkalosis respiratorik
tdk terkompensasi
@lkalosis metabolik
tdk terkompensasi @lkalosis metabolik
tdk terkompensasi
@sidosis respiratorik
terkompensasi seba,ian
@lkalosis respiratorik
terkompensasi
normal
@lkalosis metabolikterkompensasi
@&id /ase /alan&e 3isturban&es
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