7/9/2014 1

Gangguan Keseimbangan
Cairan dan Elektrolit
PPGD DI RSUP DR.M.DJAMIL PADANG
22 S/D 30 MEI 2007
Fluid Balance
Sensible
Perspiration
(variable)
Urine
(1200ml)
Absorption across
GI epithelium(2200ml)
Fecal loss
(150ml)
Respiratory loss and
Insensible perspiration
(1150ml)
Metabolic
Generation
(300ml)
Cell membrane
Input = Output = 2500ml
TBW
(Total Body Water)
Bayi : 75% berat badan
Usia 1 th : 65% berat badan
Dewasa
Laki2 : 60% berat badan
Wanita : 50% berat badan
KOMPOSISI CAIRAN TUBUH
Cairan tubuh(TBW) 60% BB :
Cairan intraseluler 40%(ICF)
Cairan ekstraseluler 20%: (ECF)
Plasma darah 5%
Cairan Interstitial 15%(ISF)


DISTRIBUSI CAIRAN TUBUH
ICF
40% TBW




ISF

I
N
T
R
A
V
A
S
C
U
L
A
R





ICF


Na-K
ATP ase
Na
K
water
water
water
TBW =
60% X BW (M)
50% X BW (F)

ICF : 2/3 TBW
ECF: 1/3 TBW
ISF:3/4 ECF
IV:1/4 ECF

THIRD SPACE
??

water
endothel
Cell Membrane
ECF = ISF+IV
ECF
I C F
KONSEP DASAR
REGULASI CAIRAN DAN ELEKTROLIT
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.

KONSEP DASAR
REGULASI CAIRAN DAN ELEKTROLIT
Our cells cannot move water molecules
by active transport. Move passively, in
response to osmotic gradients.

The bodys content of water or electrolytes
will rise if dietary gains exceed losses to the
environment and will fall if losses exceed
gains. Primarily hormonal regulated
KOMPOSISI ELEKTROLIT DALAM CAIRAN
TUBUH
ECFV (1/3TBW) ICFV (2/3 TBW)

Na: 135 145 mEq/L Na: 10 20 mEq/L

K: 3.5 5.0 mEq/L K: 130 140 mEq/L

Chloride: 95-105 mEq/L Mg: 20 30 mEq/L
Bicarbonate: 22-26 mEq/L Urea nitrogen: 10-20mg/dl
Calcium: 8.5- 10.0mg/dl Chloride: 3mEq/L
Mg: 1.4 2.1 mEq/L
Glucose: 90-120 mg/dl
Urea nitrogen: 10-20mg/dl

Osmolality &Tonicity
Body fluids kept within a narrow osmolality
range of 285295 mOsm/kg mOsm/L = mEq/L
Osmolality = mOsmol/ kg
Osmolarity= mOsmol/L
Serum Na is the main determinant of ECF osmolality

Calculated ECF osmolality (mOsm/kg)=
2x [Na
+
] + Glucose (mmol/L) + Urea (mmol/L) or
2x [Na
+
] + Glucose (mg/dl)/18 + Urea (mg/dl)/2.8

The total amount of Na in ECF is the major
determinant of the size of ECF
Osmolality and tonicity

The ECF sodium concentration is the main
determinant of plasma tonicity.

Tonicity is the ability of the combined effect
of all solutes to generate an osmotic driving
force that cause water movement from
compartment to another.




Osmolality and tonicity
NaCl 0.9%
[Na
+
] = 154 mEq/L
[Cl
--
] = 154 mEq/L
Osmolarity = 308 mEq/L higher than (n)limit
Hypertonic fluid
Dextrose 5%
5g/dL = 50g/L = 50000mg/L = (50000:MW)/ mmol/L
= 50000/180 mmol/L = 255 mmol/L
= 255 mOsmol/L lower than (n) limit
Hypotonic fluid
Content of common IV Fluids
content D5W 0.9%
NaCl
0.45%
NaCl
3%
Na Cl
LR/Hart
manns
Gela
fundin
HES 6% SPPS
Na
(mEq/L)
--
154 77 513 130 154 154
130
160
Cl
(mEq/L
--
154 77 513 109 120 154
130
160
K
(mEq/L)
-- -- -- --
4
-- --
<1
Ca
(mEq/L)
-- -- -- -- 3 -- -- --
Osmol
arity
252 308 154 1026 273 274 310 308
pH
3.2-6.5 5.0 5.0 5.0 6.0-7.5 7.1-7.7 4.0-7.0
--
Others
Dextro
se 50g
--
-- --
Lactate
28mEq/L
Gelatin
40g/L
Starch
60g/L
Albumin
50g
KESEIMBANGAN CAIRAN DAN ELEKTROLIT
DIPENGARUHI :
Mediated by three hormones:
ADH
Aldosterone
Atrial Natriuretic Peptide
Non hormonal:
Mediated by Sympathetic activation
MORE IMPORTANT
ADH
Osmoreceptors ( hypothalamus special
cells posterior hypophysis)
monitor ECF osmotic concentration
[triggered by 2% change (6mOsm/L)]
Effects: - urinary water loss and
- concentrating the urine
- stimulates the thirst center
intake fluids
Osmoreceptors
stimulated
ADH release
thirst
Urinary water loss
water gain
Additional water
dilutes ECF,
volume
Homeostasis
restored
Water loss
Concentrates ECF
volume
Urinary water loss
Water gain
ADH release
thirst
Osmoreceptors
inhibited
HOMEOSTASIS
[Na] in ECF normal
HOMEOSTASIS
DISTURBED
[Na] in ECF
HOMEOSTASIS
DISTURBED
[Na] in ECF
Homeostasis
restored
The Homeostatic Regulation of normal [Na] in Body Fluids
Aldosterone
Secretion of adrenal cortex
Effects: (along the kidneys DCT and collecting system)
- Na reabsorption followed by Cl and water
- K loss

Response to: [K] or [Na] plasma in adrenal
cortex, or activation of renin-angiotensin system
Renin release if:
- a drop in plasma volume and BP at jxtglomerular
apparatus;
- filtrate osmotic concentration at the DCT;
- [Na] atau [K] in renal circulation.
Atrial Natriuretic Peptide(ANP)
Released by cardiac muscle fibers

Response to abnormal stretching of the atrial
walls ( BP or blood volume)

Reduces thirst

Blocks the release of ADH and aldosterone
diuresis BP and Plasma Volume no
stimulation
Blood volume and
atrial distension
ANP release
Aldosteron release
ADH release
thirst
Water loss
Na loss
thirst
Water loss
Na retention
Aldosterone
release
ADH release
Renin
secretion
and
angiotensin II
activation
HOMEOSTASIS
RESTORED
HOMEOSTASIS
RESTORED
HOMEOSTASIS
Normal ECF
volume
HOMEOSTASIS
DISTURBED
ECF volume
(by fluid or
Fluid and salt gain)
HOMEOSTASIS
DISTURBED
ECF volume
(by fluid or fluid
and salt loss)
Blood volume
and blood pressure
The Integration of Fluid Volume Regulation and [Na] in Body Fluid
Regulation of fluid and electrolytes
balance (non hormonal mediated)
ECFV depletion stimulates pressure
receptors (in the aorta and carotid sinus)
activates the sympathetic nervous system
and lead to renal retention of sodium.

Causes of Hypovolemia
With decreased ECFV
Increased Fluid (volume) loss
GI tract (diarrhea, vomiting, GI suction)
Skin (sweating, burns)
Hemorrhage (trauma, surgical)
Low sodium and water intake
Impaired (n)-capacity to retain sodium and water
Osmotic diuresis (hyperglycemia)
Renal sodium wasting
Adrenal insuffiency
With increased or normal ECFV
CCF
Cirrhosis with ascites
Increased vascular permeability



Sodium and ECFV regulation
Total ECF Na ECFV
ECFV overload signs of edematous state
Total ECF Na ECFV
ECFV depletion signs of dehydration

[Na] serum does not tell about the total amount of
Na in the ECF compartment or the size of ECFV.
The [Na] serum only tells about the amount of
water relative to the amount of sodium.




Potassium balance regulation

Input: Dietary intake, Intravenous
Output: kidneys (mainly), sweat and GI tract (small)
Almost all glomerular-filtrate-K reabsorbed
K excreted by secretion at DCT and Cort.Collect.T
through aldosterone-regulated Na-K ATPase mechanism,
triggered by Na reabsorption.
Insulin and agonist-conrtrolled Na-K ATP ase and
metabolic alkalosis K enter into the cell decrease
serum [K] decrease ratio (ECF-[K] : ICF-[K])
Decreased extracellular pH (inorganic acid) increase
serum[K] increase ratio (ECF-[K] : ICF-[K])



Disorder of water balance:
Hypernatremia

([Na
+
]>145mEq/L)
Serum osmolality >300 mosm/kg
(always associated with hypertonicity)
Signs and symptoms: not specific; altered
mental status, impaired thinking, coma,
convulsion.

Hypernatraemia([Na]>145mEq/L)

Assess ECF volume


Hypovolaemia Euvolaemia Hypervolaemia


Renal losses Renal losses Iatrogenic
Diuretics Diab.Inspidus Hypertonic saline or
Osmotic diuresis Extrarenal losses Na-bic, admintr.
Diab.Insipidus vomiting, diarrhea , Cushing syndr.
Extrarenal losses sweating, respiratory Hyperaldosteronism
Vomiting, diarrhea
Skin,Respiratory
Treatment of hypernatraemia

Low ECFV : Isotonic saline, then hypotonic fluids IV (<300ml/h) or
PO free water
High ECFV: loop diuretics, Replace with hypotonic fluids if
nessecary
Correction Na level should < 0.5mEq/L/h, or
<1.0 mMeq/L/h for acute hyper Na
Treat underlying condition e.g Diabetes Inspidus: Desmopressin
When hypovolemia has been corrected:
current TBW x current [Na] = normal TBW x normal [Na]
current TBW = normal TBW x (140/current[Na])
TBW deficit = normal TBW current TBW
= 0.6 BW (kg) current TBW
= (0.6xBW)(1 140/current [Na])
Hyponatraemia (Na
+
< 135 mEq/L)

Pseudohyponatraemia
Plasma osmolality normal (hyperlipidemia, hyperproteinemia)
Plasma osmolality increased (hyperglycemia, mannitol, glycerol,
glycine)

Hypotonic or True hyponatraemia
If ECFV : deficit of both TBW and salt, but more Na than
water has been lost
If ECFV : excess of both TBW and salt, but TBW is more
than total body Na
If ECFV normal : TBW has without change in total body Na.

Hyponatraemia (Na < 135 mEq/L)

measure plasma osmolality

normal or increased Hypotonic hyponatraemia

Pseudohyponatraemia Assess ECF volume






hypovolaemia euvolaemia hypervolaemia
non-renal losses SIADH Oedema states
diarrhea, vomiting hypothyroidism CCF
skin losses adrenal insufficiency renal failure
third spacing psychogenic polydipsia nephrosis
renal losses cirrhosis
diuretics, renal failure


Treatment of hyponatraemia
Low ECF
asymptomatic: replace with isotonic saline
symptomatic: replace with hypertonic saline
Normal ECF
asymptomatic: furosemide diuresis + isotonic saline
symptomatic : furosemide + hypertonic saline
High ECF
asymptomatic : furosemide diuresis
symptomatic: furosemide diuresis + hypertonic saline

Causes of Hyperkalemia
(K>5,5)

Pseudohyperkalemia: hemolysis,
leucocytosis(>50.000),thrombocytosis
(>1000000/ml)
Impaired renal excretion: renal failure,
drugs(ACE inhib., K sparing diuretics, NSAIDs)
Excess intake: K supplements, massive
transfusion)
Transcellular shifts; acidosis, b-blockers, insulin
deficiency, succinylicholine, rhabdomyolysis.
Clinical effects of hyperkalemia

CVS: tall peak T waves, prolonged PR
interval, loss of P waves, widened QRS,
VT, VF and cardiac arrest.

Neuromuscular: weakness, areflexia,
paralysis and paraesthesia
Clinical approach Hyperkalemia
Hyperkalaemia
Pseudohyperkalaemia
Haemolysis
Leucocytosis (>50.000/ml)
Thrombocytosis(>1.000.000/ml)
Impaired renal excretion
Renal failure
Drugs:
ACE inhibitors
K-sparing diuretics
NSAIDS

Transcellular shifts
Acidosis
Beta-blockers
Insulin deficiency
Succinylcholine
Rhabdomyolysis
Excess intake
K-supplement
Massive transfusion
TREATMENT of Hyperkalemia

1.Direct membrane antagonism (cardiac toxicity) :
IV Ca-gluconas, CaCl2 10% 10 ml, over 2-5 minute

2.Transcellular shift of K:
a.IV dextrose 50% 50ml + IV 5-10 unit Regular-Insulin
b.IV Na.Bicarbonate 50-100mEq infused over 5-10 min

3.Enhanced clearance from body
- diuretics: IV frusemide 10-20mg
- haemodialysis/CRRT
- ion exchange resins (Resonium A PO 15g q 8h or
enema 30g q8h)

Hypokalemia (K<3,5)
Transcellular shifts:
insulin, glucose, beta-agonist, alkalosis

Renal K saving ( urine K<30mEq/L)
G-I losses: diarrhea, nasogastric

Renal K wasting ( urine K >30mEq/L)
diuretics, Mg depletion, dehydration,
Mineralocorticoid excess,
Alkalosis,
Amphotericin-B
Clinical effects and th/ of hypokalemia
CVS: fattened or inverted T Waves, U waves,
Arrhytmia (in digitalis th/. Or Mg)

Neuromuscular: muscle weakness, ileus and
paralysis.

Renal: Nephrogenic Diabetes Insipidus.

TREATMENT:
Replacement rate 10-30 mEq/h diluted in 100-
200 NS/D5% ( central vein)


Thank You
for your attention