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Fluid, Electrolytes, and

Acid-Base Homeostasis
Kurniawan Taufiq Kadafi

Child Health Department


Medical Faculty of Brawijaya University,/Saiful Anwar Hospital
Malang
Indonesia
Outline
• Water Homeostasis

• Sodium Homeostasis

• Potasium Homeostasis

• Calcium Homeostasis

• Magnesium Homeostasis

• Phosphate Homeostasis

• Acid Base Homeostasis


Water Homeostasis
Function of Water in the Body
• The medium in the biological activities of the body

• Transport of Nutrition and Oxygen

• Excretion of waste products

• Communication at the cellular level,

• Digestion of Food

• Regulation of body temperature

• Joint lubricants

• Electrolyte homeostasis

Barry M. Popkin, Kristen E. D Anci, Irwin H. Rosenberg, 2011; Efraín Riveros-Perez,∗, Ricardo Riveros, 2017
Body Fluid Composition
Body Fluid Composition
The human body is composed of 42%-75% water

2/3 Intracellular

3/4 Intestitial 1/3 Extracellular

1/4 Plasma
Body Fluid Composition

https://thecaribbeancurrent.com/essential-minerals-in-our-body-part-ll-potassium-sulphur/
Total Body Water
Total&body&water,&intracellular&fluid&and&extracellular&fluid&as&a&p
of&body&weight&and&a&function&of&age

*'PostQna

#
*
Cellula

#'Sex'diff

The'body'fluids'in'pediatrics.'Winter
Total Body Water
Umur Total cairan tubuh
terhadap berat badan
(%)
Bayi baru lahir 77
6 bulan 72
2 tahun 60
• \ 16 tahun 60
20 – 39 tahun
Pria 60
Wanita 50
40 – 59 tahun
Pria 55
Wanita 47
Water Homeostasis
• Maintenance of body water : Intake and Output

• Fluid intake is regulated by thirst

• Water output is primarily regulated by vasopressin at

the level of the kidney

• Thirst and Vasopresin are regulated by Plasma

Osmolality and Blood Pressure/volume status


Andrea Kelly, Thomas Moshang Jr, 2016
Water Homeostasis
• Plasma Osmolality

Andrew C. Argent, John H. Arnold, Katherine V. Biagas et al, 2016


Water Homeostasis
• Blood Pressure, Effective ECF

Andrew C. Argent, John H. Arnold, Katherine V. Biagas et al, 2016


Vasopresin
Sodium Homeostasis
Sodium Homeostasis
• Sodium plays a key role in maintaining ECF volume and
blood pressure

• The factors that influence sodium regulation:

• Natriuretic factors

• Renin-Angiotensin-Aldosterone system (RAAS)

• The sympathetic nervous system


Andrea Kelly, Thomas Moshang Jr, 2016
Sodium Homeostasis
• Natriuretic factors

Atrial myocytes release ANP in response to

distention of the cardiac atria, as occurs in the

setting of fluid overload

Andrea Kelly, Thomas Moshang Jr, 2016


Sodium Homeostasis
• Renin-Angiotensin-Aldosterone system (RAAS)

Decreases in circulating blood volume/blood

pressure detected by baroreceptors in the renal

arterioles, extrarenal baroreceptors, and the renal

macula densa stimulate renin release from the


renal juxtaglomerular cells.

Andrea Kelly, Thomas Moshang Jr, 2016


Cellular Responses to Disturbances in
Plasma Osmolality

• Hyperosmolar ECF

• Hypoosmolar ECF

Andrea Kelly, Thomas Moshang Jr, 2016


Cellular Responses to Disturbances in
Plasma Osmolality
• Hyperosmolar ECF

Andrea Kelly, Thomas Moshang Jr, 2016


Cellular Responses to Disturbances in
Plasma Osmolality
• Hypoosmolar ECF

Andrea Kelly, Thomas Moshang Jr, 2016


Renal Regulation
Renal Regulation
Renal Regulation
Potasium Homeostasis
Potasium Homeostasis
• The ICF contains nearly 98% of total body (40-50

mEq/kg) K +

•K + concentration of 140-150 mEq/L

• The concentration of K in the ECF, the site of the


+

remaining 2% of total body K

• Ranges from 3.5 to 5.5 mEq/L


Andrea Kelly, Thomas Moshang Jr, 2016
Calsium Homeostasis
Calcium Regulation
Calcium Composition
99%

Skeleton

1% Soft Tissue and


Extracellular Space

Andrea Kelly, Thomas Moshang Jr, 2016


Calcium Regulation
• Regulation in the GIT

• Regulation in the Kidney

• Hormonal Regulation

Melanie P. Hoenig and Mark L. Zeidel, 2014


Calcium Regulation in the GIT
Calcium Regulation in the GIT
• Calcium absorption in the gastrointestinal tract via active
transport is regulated by 1,25 dihydroxyvitamin D

• Calcium absorption in the duodenum and upper jejenum

• The efficiency of calcium absorption is increased with


reduced dietary intake, rapid growth during childhood,
pregnancy, and lactation.

Andrea Kelly, Thomas Moshang Jr, 2016


Calcium Regulation in the Kidney
Calcium Regulation in the Kidney

10-15% Ca
(PTH Regulation)
70% Ca

15-20% Ca < 5% Ca

(Kenneth J Banasiak, Thomas OC, 2008)


Hormonal Regulation
Hormonal Regulation
• Parathyroid Hormone

• Vitamin D

• Calcitonin

(Kenneth J Banasiak, Thomas OC, 2008)


Parathyroid Hormone
• Parathyroid Hormone (PTH) is synthesized in theparathyroid gland

• PTH enhances transcellular reabsorption of calcium in the DCT and


paracellular reabsorption in the cortical thick ascending loop of Henle

• PTH stimulates the conversion of 25-hydroxyvitamin D to 1,25(OH) D 2 3

in the proximal tubule

• PTH enhances release of calcium from bone by increasing expression


of the surface protein RANK

(Kenneth J Banasiak, Thomas OC, 2008)


Parathyroid Hormone
Vitamin D
• Vitamin D is obtained from two primary sources:
the skin and dietary supplementation

• 1,25-Dihydroxyvitamin D acts to enhance calcium

absorption primarily in the intestine

• 1,25-dihydroxyvitamin D has been shown to

decrease transcription of PTH


(Kenneth J Banasiak, Thomas OC, 2008)
Calcitonin
• Calcitonin has been shown to inhibit renal tubular
reabsorption of calcium and osteoclast-mediated bone
resorption

• The secretion of calcitonin is stimulated by increased


blood calciumlevels and by glucocorticoids, calcitonin
gene-related peptide, glucagon, enteroglucagon, gastrin,
pentagastrin, pancreozymin, and -adrenergic agents
β

(Kenneth J Banasiak, Thomas OC, 2008)


Endocrine Regulation of

6
E R

Calcium, Phosphate, and


Bone Metabolism 636 PART IX ENDOCRINE PHYSIOLOGY

Daniel E. Peavy, Ph.D. Cells mg/day of calcium excreted in the urine represent
11,000 mg about 1% of the calcium initially filtered by the kid
the remaining 99% is reabsorbed and returned to the b
Therefore, small changes in the amount of calcium
sorbed by the kidneys can have a dramatic impact on
INE
Calcium in diet cium homeostasis.
1,000 mg/day Bone
1,000 g
Phosphate Handling by the GI Tract, Kidneys, and B
IUM AND PHOSPHORUS IN ■ REGULATION OF PLASMA CALCIUM AND Figure 36.2 shows the overall daily flux of phosphate i
PHOSPHATE CONCENTRATIONS body. A typical adult ingests approximately 1,400 m
UM AND PHOSPHATE ■ ABNORMALITIES OF BONE MINERAL
of phosphorus. In marked contrast to calcium, most (
Absorption Deposition mg/day) of this phosphorus is absorbed from the GI
METABOLISM 300 mg/day 500 mg/day
Extracellular
typically as inorganic phosphate. There is an oblig
fluid contribution of phosphorus to the contents of the GI
Secretion 900 mg Resorption (about 200 mg/day), much like that for calcium, result
150 mg/day 500 mg/day a net uptake of phosphorus of 1,100 mg/day and excr
TS of 300 mg/day via the feces. Thus, the majority of ing
phosphate is absorbed from the GI tract and little p
Glomerular through to the feces.
filtrate Reabsorbed
els fall below normal, sponta- vital role in calcium and phosphate homeostasis, and actsmg/day
9,850
10,000 mg/day
n be generated in nerves, lead- on bones, kidneys, and intestine to raise the plasma cal-
Cells
which, if severe, can result in cium concentration and lower the plasma phosphate con-
Fecal excretion 84 g
centration. 850 mg/day
g calcium is in the free or ion- 5. Vitamin D is converted to the active hormone 1,25-dihy- Kidney
und to small anions, and about droxycholecalciferol by sequential hydroxylation reactions
oteins. Most of the phosphorus in the liver and kidneys. This hormone stimulates intestinal
Phosphorus in diet
sphate. calcium absorption and, thereby, raises the plasma cal-
1,400 mg/day Bo
alcium is not absorbed by the GI cium concentration. 50
via the feces; by contrast, phos- 6. Calcitonin, a polypeptide hormone produced by the thyroid
y absorbed by the GI tract and glands, tends to lower the plasma calcium concentration,
the urine. but its physiological importance in humans has been ques-
ormone (PTH), a polypeptide tioned. Absorption Deposition
parathyroid glands, is stimu- 7. Osteoporosis, osteomalacia and rickets, and Paget’sUrinary
diseaseexcretion
1,300 mg/day 200 mg/day
150 mg/day
ma-ionized calcium. PTH plays a are the most common forms of metabolic bone disease. Extracellular
Magnesium Homeostasis
Magnesium Regulation
Magnesium Regulation
• Regulation in the GIT

• Regulation in the Kidney

Andrea Kelly, Thomas Moshang Jr, 2016


Magnesium regulation in the GIT
Magnesium regulation in the GIT

• Dietary magnesium is principally absorbed in the

jejunum and the ileum by both active and passive

mechanisms

• Magnesium absorption is enhanced during

reduced dietary intake

Andrea Kelly, Thomas Moshang Jr, 2016


Magnesium regulation in the
Kidney
Magnesium regulation in the GIT

5-10% Mg
(PTH regulation)
5-15% Mg

3% Mg
60-70% Mg

Andrea Kelly, Thomas Moshang Jr, 2016


Phospate Regulation
• Regulation in the GIT

• Regulation in the Kidney

• Hormonal Regulation

Melanie P. Hoenig and Mark L. Zeidel, 2014


Calcium Regulation in the GIT
Phospate regulation in the GIT
• Phosphate is absorbed in the duodenum and

jejunum by passive processes and active

mechanisms regulated by 1,25-dihydroxyvitamin

D.

Andrea Kelly, Thomas Moshang Jr, 2016


Calcium Regulation in the Kidney
Phospate regulation in the GIT

80% P
(PTH regulation)

3%-20% P
5% P

Andrea Kelly, Thomas Moshang Jr, 2016


Hormonal Regulation
Parathyroid Hormone
• Parathyroid Hormone (PTH) secretion can be
stimulated directly by markedly elevated levels of

phosphate

• Elevated blood phosphate indirectly stimulates


PTH secretion by reducing blood calcium and 1,25-

dihydroxyvitamin D levels

(Kenneth J Banasiak, Thomas OC, 2008)


Acid Base Homeostasis
blood gas analysis

ACIDOSIS ALKALOSIS
7.35-7.45

pH

45-35

PCO2

22-26 -3 to +3

HCO3-or BE
Pendekatan
Handerson-Hasselbach vs Stewart
Pendekatan Henderson-Hasselbach

1868-1939 Sorensen menemukan notasi pH



Henderson menemukan perhitungannya

Hasselbach mengadaptasikan keduanya dalam suatu formula

HCO3
Normal [HCO
BASA
GINJAL
3
-] HCO3

pH = 6.1 + log Kompensasi


Normal pCO2
αPARU
ASAM
CO
CO 2 2
stewart method
pH atau H+ dalam plasma ditentukan oleh

Variabel independen Variabel dependen

pCO2, SID, Atot HCO3-


stewart method

PCO2 H +

SID OH -

Atot HCO3 -
pCO2 role
PCO2 role

H2O + CO2 H2CO3 H+ + HCO3-

CO2
production
VCO2
PaCO2 ∝
VA Alveolar
ventilation
Strong Ion Difference
Ionic role

Strong ion Weak ion

Na + Albumin
K + PO4 -

Ca 2+ HCO3 -

Mg 2+

Cl -
law of conservation mass

Cation Anion
STRONG ION DIFFERENCE IN PLASMA
ELECTRONEUTRALITY

H+ OH- CO 32-

[SID]
HCO3-

CHANGE IN PH OR [H+] AS A Weak acid


CONSEQUENCE OF WATER Na+ Alb -

Posfat -
DISSOCIATION IN RESPONSE UNMEASURED ANION
TO CHANGE IN [SID], PCO2 UA - Mostly lactate and ketones
AND WEAK ACID

K+
Mg ++
Ca++
Cl -

CATION ANION
George 2015
strong ion difference
Mg2+ Unmeasured
anion+
SIG
Ca2+

K+ SIDa Phospate
40-42 meq/l Albumin SIDe
HCO3-
Lactate

Na+
140 meq/l
Cl-
100 meq/l
EASY WAY TO UNDERSTAND STEWART’S ACID-BASE

STRONG ION GAP (SIG)


Mg++
Ca++ UA SIG
K+ 4
SIDa HCO3-
A-
SIDe
Lactate

SIDa = [Na+] + [K+] + [Mg++] + [Ca++] - [Cl-] – [Lactate-]

+ Cl -
SIDe Na )+10×[alb]×(0.123×pH–0.631)
= 12.2×pCO2/(10-pH +[PO4–]×(0.309×pH–0.469)

SIG = SIDa – SIDe Normal value = zero

CATION ANION
Kellum JA, Kramer DJ, Pinsky MR: Strong ion gap: A methodology for exploring unexplained
anions. J Crit Care 1995,10:51--55.
strong ion difference

acid base

Kellum, Crit care 2000


CATION ANION

STRONG ION DIFFERENCE IN WATER

[H+] [H+] [OH-]


Acidosis Alkalosis

OH-
OH-
OH-

Na Cl Na Na
Cl Cl

(–) [SID] (+)


THE RELATIONSHIP BETWEEN [SID] AND pH/[H+]
Asam Lemah Total
weak ion

Atot = A- + AH

Most of weak ion (negative charge)


is protein (albumin)
renal regulation in acidosis

Cl-
renal regulation in alkalosis
intestinal regulation
Na#
Cl#

Cl#
Na#

Na# Plasma)SID)in)gastric)site)
Cl#

Cl# Plasma)SID)in)duodenum)site)
Na#

Na#
Cl# Plasma)SID)in))colon)site)

Regional)
Perfussion)
acid base diagnosis
Acidosis Alkalosis
Respiratory ↑PCO2 ↓PCO2
Non respiratory (metabolic)

1. Abnormal SID

a. Water excess/deficit ↓SID,↓[Na+] ↑SID,↑[Na+]


b. Imbalance of strong anion

i. Chloride excess/deficit ↓SID,↑[Cl-] ↑SID,↓[Cl-]


ii. Unidentified anion excess ↓SID,↑[XA-] -
2. Nonvolatile weak acids

a. Serum albumin ↑[Alb] ↓[Alb]


b. Inorganic phosphate ↑[Pi] ↓[Pi]
respiratory etiology

Acid-base
Type of disorder Pathogenesis Etiology
disorder

1.CNS depression
Hypoventilation ↑PCO2 Acidosis
2.NMD

1.CNH
Hyperventilation ↓PCO2 Alkalosis 2.Psychiatric disorder
3.Improper MV setting
non-respiratory etiology

Type of Acid-base
Pathogenesis Etiology
disorder disorder

1.High chloride infusion


Abnormal
↑[Cl-] or
2.Post-pyloric loss
Acidosis
SID 3.RTA, tubulopathy
↓[Na+] 4.Water excess

1.Endogenous:lactate,
ketone, sulfate, IEM
↑[XA-] 2.Exogenous:salicylate,etha
nol, methanol
non-respiratory etiology

Type of Acid-base
Pathogenesis Etiology
disorder disorder

1.Chloride responsive:GI
Abnormal loss, renal loss
SID
Alkalosis ↓[Cl-] 2.Chloride non-responsive:
mineralocorticoid excess

1.High Na infusion
↑ [Na+] 2.Water loss
non-respiratory etiology

Type of Acid-base
Pathogenesis Etiology
disorder disorder

Abnormal
↑[Alb], Excessive exogenous
Acidosis phosphate or albumin
Atot
↑[Pi]

↓[Alb], Nephrotic syndrome, hepatic


cirrhosis
↓[Pi]
ABNORMAL IN SID AND WEAK ACID
K
Mg [SID]
[SID] [SID]
Ca [SID]=34
[SID]
Alb Laktat/keto [SID]
PO4 Alb/
Alb Alb
PO4
PO4
PO4
Alb
Na PO4

140

Cl Cl CL Cl Cl Cl
102 115 95 102 102 102

Normal Hyperchlor Hypochlor Keto/lactate Hypoalb/ Hyperalb/


acidosis fosfat fosfat
alkalosis acidosis
alkalosis acidosis

George 2015
Bagaimana Penambahan Air
bisa menyebabkan Asidosis?
Plasma

1 Liter 140/2 = 70 mEq/L


H 2O 102/2 = 51 mEq/L
Na+ = 140 mEq/L
SID = 19 mEq/L
Cl- = 102 mEq/L
SID = 38 mEq/L 1 liter 2 liter

SID : 38 ➜ 19 = Acidosis

DILUTION ACIDOSIS
CATION ANION

STRONG ION DIFFERENCE IN WATER

[H+] [H+] [OH-]


Acidosis Alkalosis

OH-
OH-
OH-

Na Cl Na Na
Cl Cl

(–) [SID] (+)


THE RELATIONSHIP BETWEEN [SID] AND pH/[H+]
plasma + NaCl 0.9%

Plasma NaCl 0.9%

Na+ = 140 mEq/L Na+ = 154 mEq/L


Cl- = 102 mEq/L Cl- = 154 mEq/L
SID = 38 mEq/L 1 liter SID = 0 mEq/L 1 liter

SID : 38 ➜
plasma + NaCl 0.9%

Plasma

= Na+ = (140+154)/2 mEq/L= 147 mEq/L


Cl- = (102+ 154)/2 mEq/L= 128 mEq/L Hiperchloremia
SID = 19 mEq/L 2 liter

SID : 19 ➜ Acidosis
ABNORMAL IN SID AND WEAK ACID
K
Mg [SID]
[SID] [SID]
Ca [SID]=34
[SID]
Alb Laktat/keto [SID]
PO4 Alb/
Alb Alb
PO4
PO4
PO4
Alb
Na PO4

140

Cl Cl CL Cl Cl Cl
102 115 95 102 102 102
128
Normal Hyperchlor Hypochlor Keto/lactate Hypoalb/ Hyperalb/
acidosis fosfat fosfat
alkalosis acidosis
alkalosis acidosis

George 2015
Terima Kasih
Mechanism of fluids movement
• Passive Transport

• Diffusion

• Osmosis

• Hydrostatic Pressure

• Active Transport

Thomas Zeuthena, Nanna MacAula, 2002; Efraín Riveros-Perez,∗, Ricardo Riveros, 2017
Passive Transport
Diffusion
Diffusion
•Gas exchange at the alveoli — oxygen from air to blood, carbon
dioxide from blood to air.

•Gas exchange for photosynthesis — carbon dioxide from air to leaf,


oxygen from leaf to air.

•Gas exchange for respiration — oxygen from blood to tissue cells,


carbon dioxide in opposite direction.

•Transfer of transmitter substance — acetylcholine from presynaptic


to postsynaptic membrane at a synapse.

•Osmosis — diffusion of water through a semipermeable membrane.


Osmosis
Osmosis
•Re-absorption of water by the proximal and distal

convoluted tubules of the nephron.

•Re-absorption of tissue fluid into the venule ends of the

blood capillaries.

•Absorption of water by the alimentary canal — stomach,

small intestine and the colon.


Hydrostatic Pressure
Active Transport
Transport Na-K Pump ATPase

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