Introduction to body fluid

composition and basic physiology of

fluid balance
DISTRIBUSI CAIRAN TUBUH

Best Practice & Research Clinical Anaesthesiology 23 (2009) 145–157

Kompartemen tubuh dan distribusi pada masing2
kompartemen
ECF endothel
I TBW =
ICF
Cell Membrane
Na N
60% X BW (M)
Na-K T
40% TBW ATP ase R 50% X BW (F)
K A
water V
water A ICF : 2/3 TBW
nucleus water S ECF: 1/3 TBW
water C ISF:3/4 ECF
U
ICF ISF L IV:1/4 ECF
A
R THIRD SPACE
??
ICF ECF = ISF+IV
 JUMLAH CAIRAN
UMUR JENIS KELAMIN JUMLAH
( % BB)
0 – 1 bulan 75,7
1 – 12 bulan 64,5
1 – 10 tahun 61,7
10 – 16 tahun Laki 58,9
Perempuan 57,3
17 – 19 tahun Laki 60,6
Perempuan 50,2
40 – 59 tahun Laki 54,7
Perempuan 46,7
> 60 tahun Laki 51,5
Perempuan 45,5
 Body Fluids/ Water
• Provide transportation of nutrients, oxygen to
cells

• Carry waste products away from cells

• Provide environtment for electrolyte chemical

reactions to occur
Solute Distribution in Fluid Compartments
(Cations and Anions in Body Fluids)
Figure 27.2
 Ionic Composition of Body Fluids
Electrolyte Plasma (mEq/L) Plasma water Interstitial Intracellular
(molarity) (mEq/kg)(molality) Fluid (mEq/L) Fluid (mEq/L)

Cations
Sodium 142 153 145 10
Potassium 4 4.3 4 160
Calcium 5 5.4 5 2
Magnesium 2 2.2 2 26
Total Cations 153 165 156 198
Anions
Chloride 101 108.5 114 3
Bicarbonate 27 29 31 10
Phospahate 2 2.2 2 100
Sulphate 1 1 1 20
Organic acid 6 6.5 7
Protein 16 17 1 65
Total Anions 153 165 156 198
 ZAT OSMOLAR PLASMA INTER’TIAL INTRA SEL
Na + 142 (mOsm/L) 139 (mOsm/L) 14 (mOsm/L)

K+ 4,2 4,0 140

Ca++ 1,3 1,2 0

Mg++ 0,8 0,7 20

Cl- 108 108 4

HCO3- 24 28,3 10

HPO4-, H2PO4- 2 2 11

SO4= 0,5 0,5 1

Phosphocreatin - - 45

Carnosine - - 14

Asam amino 2 2 8

Creatine 0,2 0,2 9

Lactate 1,2 1,2 1,5

Adenosine triphosphat - - 5

Hexose monophospahte - - 3,7

Glucose 5,6 5,6 T Book o-f

Protein 1,2 0,2 hysiolog4y
P
Urea 4 G uyton, 20406
4
Lain lain 4,8 3,9 10
Keseimbangan Input = Output = 2500ml
cairan
Respiratory loss and Sensible
Insensible perspiration Perspiration
Fecal loss (variable)
(1150ml)
(150ml)

Metabolic Urine
Generation (1200ml)
(300ml)

Cell membrane Absorption across

GI epithelium(2200ml)
 Pergerakan cairan & Molekul
• Osmosis
• Difusi
• Filtrasi
• Transpor aktif
 ISOTONIC SOLUTIONS
• Same solute concentration as blood

• If injected into vein: no net movement of fluid

 Hypertonic solutions
• Higher solute concentration than blood
• If injected into vein:
- Fluid moves from interstitial space INTO vein
 Hypotonic Solutions
• Lower solute concentration than blood
• If injected into vein:
Fluid moves OUT of veins into tissues
RuSpwteullriend
g
cecellll
 Keseimbangan cairan intravaskular dan
interstisial

• Starling Hypothesis

• Endothelial Glycocalyx Layer

 HIPOTESA STARLING (1896)
• ReĐall StarliŶg’s Laǁ of the Capillaries ǁ h i Đh edžplaiŶs
fluid and solute movements from Ch. 19

Dalam keadaan normal terjadi ͞perembesan͟ cairan

dari intravaskuler ke ekstravaskuler.
 SISTEM LIMFE DI KAPILER

Sistem limfe mencegah

terjadinya penumpukan cairan di
interstitial sehingga tidak terjadi
edema.
͞Douďle Barrier CoŶĐept͟
 ENDOTHELIAL GLYCOCALYX LAYER
(EGL)
• Lapisan yang melapisi bagian dalam endothel.
• Ketebalan lapisan : 50 nm.
• Terdiri dari :
– Proteoglycan sulfat
– Hyaluronan
– Glycoprotein
– Protein plasma
 FUNGSI EGL
• Fungsi barier kapiler
• Mencegah adhesi leucocyte dan agregasi
thrombocyte.
• Mencegah terjadinya reaksi inflamasi.
• Mencegah terjadinya edema.
ENDOTHELIAL GLYCOCALYX LAYER
(EGL)

1).J Cereb Blood Flow Metab 2000; 20:1571–8

2).Annu. Rev. Biomed. Eng. 2007. 9:121–67
 PERBEDAAN STARLING dan EGL teori
PRINSIP STARLING
• Perbedaan tekanan onkotik
antara intra vaskuler dan
interstitial berperan
terjadinya ͞filtrasi͟ cairan ke
interstitial.
ENDOTHELIAL GYCOCALYX
LAYER
• Perbedaan tekanan onkotik
antara intra vaskuler dan
interstitial tidak berpenga-
ruh terjadinya ͞filtrasi͟
cairan ke interstitial.
• Keutuhan EGL lebih
berperan terjadinya
͞filtrasi͟ tersebut.
Fluid Shifts

Type • The physiologic shift (colloid-

free, shift of fluid & electrloytes)
• Vascular barrier is intact
1 • E/ Increased Hidrostatic pres.

Type • The Pathologic shift (fluid

containing protein
• Altered func.Vasc. Barrier
2
 PEREMBESAN CAIRAN
1. Tipe I:
– Disebut : ͞phLJsiologiĐshift͟.
– Terjadi pada keadaan normal (dinding kapiler
dalam keadaan utuh).
– Berisi air dan elektrolit (tidak mengandung
protein).
– Disebabkan karena tekanan hidrostatik ↑ ;infus
cairan kristaloid yang berlebihan).
 PEREMBESAN…. (lanjutan)
2. Tipe II:
– Disebut ͞pathologiĐshift͟
– Terjadi apabila EGL mengalami kerusakan.
– Berisi cairan yang mengandung protein.
– Penyebab kerusakan EGL:
• Pembedahan (lama dan ͞ďerat͟ŶLJa tindakan).
• Stres mekanik .
• Endotoksin.
• Iskhemia-reperfusion injury.
• Hipervolemia akut sehingga keluar ANP.
• Mediator peradangan yang lain
 Konsep2 dasar pengaturan elektrolit dan cairan

• All the homeostatic mechanisms that monitor and

adjust the composition of body fluids respond to
changes in the ECF, not in the ICF.
(plasma and CSF detect significant changes in
composition or volume and trigger appropriate neural
and endocrine responses).

• No receptors directly monitor fluid or electrolyte

balance. But our receptors can monitor plasma volume
and osmotic concentration.
• Extracellular fluid balance is maintained
through closely regulated loss and retention
to ensure that the total level of fluid in the
body remain constant.
Relationship Between Fluid Volume &
Renal Perfusion
The Integration of Fluid Volume Regulation and [Na] in Body Fluid
 Blood volume and  ANP release  Aldosteron release
 atrial distension
ADH release

HOMEOSTASIS
 thirst
DISTURBED
 ECF volume
 Water loss
 (by fluid or HOMEOSTASIS
 Fluid and salt gain) RESTORED
 Na loss
HOMEOSTASIS
Normal ECF
volume HOMEOSTASIS  thirst
RESTORED
HOMEOSTASIS
DISTURBED
 Water loss
 ECF volume
(by fluid or fluid
 Na retention
and salt loss)
 Renin
 Aldosterone
secretion
release
and
 Blood volume
angiotensin II
and blood pressure
activation  ADH release
The Integration of Fluid Volume Regulation and [Na] in Body Fluid

Osmoreceptors  ADH release  Urinary water loss

 thirst  water gain
stimulated

HOMEOSTASIS
DISTURBED
[Na] in ECF Additional water
Homeostasis dilutes ECF,
restored volume
HOMEOSTASIS
[Na] in ECF normal
Homeostasis
restored Water loss
Concentrates ECF
HOMEOSTASIS
volume
DISTURBED
[Na] in ECF

Osmoreceptors  ADH release Urinary water loss

inhibited  thirst  Water gain

The Homeostatic Regulation of normal [Na] in Body Fluids

Atrial Natriuretic Peptide (ANP)
Peregangan Atrium berlebihan → Sekresi ANP
→ Peningkatan GFR → Penurunan reabsorbsi
Na → Peningkatan eksresi garam dan air
 Kesimpulan
• Diatribusi air dalam tubuh: Intrasel (ICF), Ekstrasel
(ECF),Interstitial, Intravaskular dan Transelular
• Kandungan kristalloid dan kolloid memberikan peran
osmolalitas peran tekanan osmotik dan onkotik
• Perubahan osmolalitas dan volume ECF memicu reaksi
neurohormonal (ADH, ANP, Aldosteron) untuk
menjaga homeostasis cairan tubuh
• Perpindahan cairan anta Intravaskular dan interstitial
- fisiologis (Starling)
- patologis (Kerusakan glycocalyx)
Terima Kasih
Regulasi oleh sistim hormon terhadap
keseimbangan cairan dan elektrolit

Di atur oleh 3 jenis hormon :

• ADH
• Aldosterone Paling penting

• Atrial Natriuretic Peptide

Pengaturan Non hormonal:

Melalui aktivasi sistim sympatis
Efek ADH
• Menurunkan cairan yg dikeluarkan lewat urin
• Meningkatkan konsentrat urin
• Menstimulasi pusat haus (thirst center) →
intake fluids
• Osmoreceptors ( hypothalamus special cells
→ posterior hypophysis) akan memonitor
konsentrasi osmotik ECF [triggered by 2%
change (6mOsm/L)]
 Aldosterone
• Disekresikan oleh kortex adrenal
Efek : ;aloŶg the kidŶeLJ’s DCT aŶd ĐolleĐtiŶg sLJsteŵͿ
- reabsorpsi Na → diikuti dengan Cl dan air
- K loss
• Akan memberikan respons terhadap :  [K] or  [Na]
plasma pada kortex adrenal, dan mengaktifkan sistim
renin-angiotensin
Pelepasan Renin terjadi pada :
-penurunan plasma volum dan tek darah pada juxtglomerular
apparatus;
Threshold volume receptor: terjadi bila terdapat
perubahan volume darah sebanyak → 7-10%
-  filtrate osmotic concentration at the DCT;
- [Na] atau [K] in renal circulation.
 πi Pi

Pv Vascular Lumen πv
ESL
EG
π ESL
PENGATURAN VOLUME CAIRAN TUBUH
 FLUID RESPONSIVENESS

Erwin Pradian
Department of Anesthesiology & Intensive Care
Santosa Hospital Bandung Central
1
 Kasus
• Pria 55 th, Decomp Cordis, riwayat HHD.
– ICU, edema paru
– Apatis-CM, ekst dingin, HR 120, RR 10 (SIMV 10, PS 10, PEEP 5,
FiO2 50%), BP 110/55, S 37.8. Ronki +/+, kardiomegali

– Lab; 11,6/11.000/36/239. GD; 180, U/C 95/2.3

– Th/ lasik drip 10 mg/jam , NTG, lanoxin
– Oliguri (0.2 cc/kg/BB)
– AGD 7.48/46/81/+9.1/96% dgn 40% O2.
– Na 133, K 2.9 Cl 90, Alb 3.5
 Can’t I look at my patient and
tell if they are OK?

NO! Physical Assessment is often inaccurate,

slow to change and difficult to interpret

3
 Fluid responsiveness
• Definisi:
• Penilaian respon peningkatan curah
jantung setelah pemberian cairan.

4
 Definisi Syok
• Suatu kondisi fisiologis yang
mengakibatkan perfusi organ dan
oksigenasi jaringan tidak adekuat

Gangguan Fungsi
IT IS NOT
LOW BLOOD
PRESSURE !!!
Gagal Organ
IT IS
HYPOPERFUSION…..
Kematian
5
 Statement of the Problem
Endpoint Resuscitation

Traditional Normalizatio Compensated

Marker n SHOCK
of Vital Sign
Urine Output

INADEQUATE OXYGENATION
Scalea TM, Maltz S, Yelon J, et al.
Crit Care Med 1994; 22:1610-1615

6
 References
Inaccuracies of Physical Assessment
• Connors AF Jr, Dawson NV, Shaw PK, Montenegro HD, Nara AR, Martin L.
Hemodynamic status in critically ill patients with and without acute heart disease.
Chest. 1990 Nov;98(5):1200-6.
• Dawson NV, Connors AF Jr, Speroff T, Kemka A, Shaw P, Arkes HR. Hemodynamic
assessment in managing the critically ill: is physician confidence warranted? Med
Decis Making. 1993 Jul-Sep;13(3):258-66.
• Eisenberg PR, Jaffe AS, Schuster DP. Clinical evaluation compared to pulmonary
artery catheterization in the hemodynamic assessment of critically ill patients. Crit
Care Med. 1984 Jul;12(7):549-53.
• Iregui MG, Prentice D, Sherman G, Schallom L, Sona C, Kollef MH. Physicians'
estimates of cardiac index and intravascular volume based on clinical assessment
versus transesophageal Doppler measurements obtained by critical care nurses. Am
J Crit Care. 2003 Jul;12(4):336-42.
• Neath SX, Lazio L, Guss DA. Utility of impedance cardiography to improve physician
estimation of hemodynamic parameters in the emergency department. Congest
Heart Fail. 2005 Jan-Feb;11(1):17-20.
• Staudinger T, Locker GJ, Laczika K, et al. Diagnostic validity of pulmonary artery
catheterization for residents at an intensive care unit. J Trauma. 1998
May;44(5):902-6.

7
Are Physical Signs Early or Late
Indicators of Clinical Status?
Which signs are
Signs of similar with all
Hypoperfusion three?

LV dysfunction BP

Hypovolemia HR

Sepsis LOC

Urine output

8
 Acute Hypoperfusion
↑ Blood Lactate
Imbalance between
O2 demand and O2 delivery

MOFS

9
10
 Does CVP and PAOP tell us about
blood volume and flow?
• CVP and PAOP should never be used in
isolation
– Inconsistent in revealing information about volume
and flow
• Flow and pressure do not always correlate
– Marik et al. Based on the results of our
systematic review, we believe that CVP should no
longer be routinely measured in the ICU,
operating room, or emergency department.

Marik P, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness?
A Systematic Review ofthe Literature and the Tale of Seven Mares. Chest 2008;134;172-178
11
BP Measurement - Useful or
Misleading?
• Is BP is measured because it can be measured
• If BP increases, does blood flow increase?
– think of use of Vasopressor
• Blalock 1943, says:
“It is well known by those interested in this
subject that the blood volume and cardiac
output are usually diminished in traumatic
shock before the arterial blood pressure
declines significantly”
Blalock A, (1943) Surgery 14: 487-508

12
Blood Pressure and Blood
Flow
Do they equal each other?

13
 Physiology Background
• Oxygen delivery components
– Cardiac output x oxygen saturation x hemoglobin
• Cardiac output components
– Stroke volume
• Preload
• Afterload (Systemic Vascular Resistance)
• Contractility
– Heart rate
• Primary methods to increase cardiac output
– Increase preload (volume expanders)
– Increase contractility (inotropes)
– Decrease afterload (vasodilators)
• Key point
– Administering volume may increase intravascular volume and preload but
not stroke volume and cardiac output
 BP = CO x SVR

• CO = Stroke volume x heart rate

– decrease in SV causes increase in heart
rate
– decrease in CO causes increase in SVR
• Compensatory changes keep the BP
close to normal initially in shock states
• BP does not change until late due to
these compensatory responses
15
 Temporal order of events
(each event can take minutes to hours)

• Stroke volume falls

• Heart rate compensates to keep cardiac output
normal
– Many reasons for heart rate to increase
• Cardiac output falls
• Heart rate compensation fails
• Vasoconstriction (increase in SVR), BP remains
unchanged
• Increased oxygen extraction of
hemoglobin
• Peripheral initially (StO2)
• Central later (ScvO2)
• Blood pressure, urine output change
16
Fluid responsiveness is related to cardiac responsiveness
Cristalloids 500 – 1000 ml, or
Colloids 300 – 500 ml
Safety limit:
CVP of 15 mmHg !!
Cristalloids 500 – 1000 ml, or
Colloids 300 – 500 ml
Fluid responsiveness is related to cardiac responsiveness

Stroke volume

Fluid responsiveness

Preload
Pulse pressure variation
Stroke volume variation
SVV = SV max – SV min / SV mean
Problems with PPV and SVV

Spontaneously breathing patients

Arrhythmias
Significant tachycardia
Very low tidal volumes
Passive Leg Raising

Venous blood from legs and abdomen increases preload

İt is just like fluid challenge but it is reversible

Needs real time CO monitoring
 PLR compared with volume expansion
Post Volume
Baseline 1 PLR Baseline 2 expansion

HR HR HR HR
SV SV SV SV
VF VF VF VF

SPONTANEOUSLY BREATHİNG PATİENTS

500 ml colloid infusion
ALERT: Do not use PLR in patients with abdominal hypertension

NT
 Echocardiography to asses fluid status and responsiveness

• Static parameters
LVEDV
IVC
• Dynamic parameters
SVV with repeated SV measurements
Change in IVC/SVC diameter
septum position
• For assessment of
Heart lung interactions
Passive leg raising
Fluid challenge
 Kesimpulan

• Pemberian cairan yang berlebihan akan menyebabkan

edema yang menyebabkan peningkatan morbiditas dan
mortalitas.
• Endothelial glycocalyx mempunyai peran yang sangat
penting dalam pengaturan shifting cairan tubuh, dan
glikokaliks ini selain oleh hipoksia, stress respon, dapat juga
dirusak oleh hipervolemia akut.
• Pengukuran status cairan secara dinamis lebih akurat
dibanding pengukuran secara statis.
 Selanjutnya…..

Semoga Bermanfaat…..
Wass. Wr. Wb.
Is Cardiac Output Adequate?

Is blood flow adequate to meet metabolic demands?

Adequate Driving
Pump
intravascular pressure for
function ?
volume? venous return?
Is Cardiac Output Adequate?

We Should Know

The effects of
Left & right Preload &
respiration or
ventricular preload
mechanical
function responsiveness
ventilation
Stratification of perioperative monitoring tools

Level Conventional, ECG, NIBP,

1 non-invasive SpO2, EtCO2

Conventional, CVP, ABP

invasive

Level Minimally Oesoph Doppler,

2 invasive PCM, ScvO2

Calibrated PCM,
Less invasive ScvO2

Level Invasive PAC, SvO 2

3
 Frank-Starling Relationship

Stroke
Volume

0
0
Preload
Role of fluids (and preload) in goal-directed therapy

DO2
(Outcome)

Fluids (ml)
Role of fluids (and preload) in goal-directed therapy

Optimal
DO2

Optimal preload
DO2
(Outcome)

Fluids (ml)
Role of fluids (and preload) in goal-directed therapy

Optimal
DO2

Optimal preload
DO2
(Outcome)

Hypovolemia

Fluids (ml)
Role of fluids (and preload) in goal-directed therapy

Optimal
DO2

Optimal preload
DO2
(Outcome)

Hypovolemia Oveload

Fluids (ml)
Role of fluids (and preload) in goal-directed therapy

Low risk patients with

no cardio-respiratory disease = ASA 1-2
Optimal
DO2
Safety margin

DO2
(Outcome)

Hypovolemia Oveload

Fluids (ml)
Role of fluids (and preload) in goal-directed therapy

High risk patients with

major cardio-respiratory disease = ASA 3-4
Optimal
DO2
Safety margin

DO2
(Outcome)

Hypovolemia Oveload

Fluids (ml)
Role of fluids (and preload) in goal-directed therapy

Optimal
DO2
Safety margin

DO2
(Outcome)

Hypovolemia Oveload

Fluids (ml)