Champs Elysées

triumphal arch
Fluid and Electrolyte
Management

Department of Gastrointestinal Surgery

Dr. Wang Ailiang
Body water and its distribution

•
•
• extracellular( Na+ ） plasma water
• 25% (5%B.W.)
• Total （ 20% body weight ） (ICF)
• body interstitial fluid
• water 75% (15%B.W.)
• intracellular (K+)
• (40% body weight) (ECF)
•
Total body water (as percentage of body
weight) in relation to age and sex

Age Male Female

10-18 59 57

18-40 61 51

40-60 55 47

Over 60 52 46
 Electrolyte composition of human
body fluids
Positive ion Negative ion (mmol/L)
(mmol/L)

ECF Na+ Ca2+<>/sup Cl- HCO3-

(plasma) 140 5 104 24

ICF K+ Mg2+ HPO42- protein

150 26 100 65
 Starling relationshilps

• Plasma proteins (album) account for the

high colloid osmotic pressure of plasma

• It’s an important determinant of distribution

of fluid between vascular and interstitial
compartments
 water electrolyte

electrolyte
water
Protein account for the
Capillary wall high colloid osmotic
pressure
Exchange of water and electrolyte
between plasma and interstitial fluid
 epicyte
ECF ICF

Ion channel

Enzym (pump)
Mechanism of kidneys to maintain constant
volume and composition of body fluids

• Filtration and reabsorption of sodium:

adjusts urinary sodium excretion to match
changes in dietary intake

• Regulation of water excretion in response to

changes in secretion of antidiuretic hormone
 Blood volume Blood volume

Blood pressure

plasma osmotic thirst plasma osmotic

pressure pressure

Reabsorption Reabsorption
of water ADH↑ ADH↓ of water

urine urine
Regulating and effect of ADH
(antidiuretic hormone)
Osmolality (290mosm/kg H O) 2

• Solutes dissolved in body fluid

contribute to total osmolality in
proportion to their molar concentration

• ECF→ sodium and its salts

• ICF→ salts of potassium

 cell cell

Movement of water

electrolyte

ECF ICF

ECF ICF

Balance of osmotic pressure between both sides of epicyte

 Control of Osmolality
• Regulation of water intake (thirst) and excretion
(urine volume, insensible loss, and stool water) ←
kidney (regulator)
• water intake↓→ kidney→ urine volume↓ urine
solute concentration↑ (fourfold above plasma 1200-
1400mosm/kg H O)22

• water intake↑→ kidney→ urine volume↑ urine

solute concentration↓ (dilute urine 50mosm/kg H O)
22
 Equation
• Osmolality ＝ (Na e++ A-)+(K e++ A- )
TBW
• PNa ＝ (Na e++K e+ )
• TBW
• Na e
+
:exchangeable sodium
• K e :
+
exchangeable potassium
• TBW: total body weight
• PNa : plasma sodium concentration
 Typical daily solute balances in normal subjects
intake Excretion

concentration Total amount concentration Total amount

water
Urinary
excretion
ingested 2L water 1.5L

0.4L
cell Total solute 400mosm/kgH2O 600mosm
metabolism
sodium 60meq/L 90meq
Total solute 600mosm
potassium 36meq/L 54meq
sodium 100meq Insensible 10ml/kg/24h
(stools ＞
Loss (water) 200ml/d)
potassium 60meq ☆

☆ External (insensible )water loss: lungs, skin, stool

Volume disorders
Volume depletion

Volume overload
Recognition and treatment of volume depletion
…… Low BP

Dry mucous membranes Clinical tachycardia

manifestation

Narrow pulse pressure Poor skin turgor

History taking for volume depletion

records Of the history

Analysis
Intake Changes Urine Of
and In Specific The
output Body gravity Chemical
weight Composition
Of
urine
History taking for volume depletion
Intake
and
Changes output
In body
weight

Treatment plan
Urine devised aiming to
Specific Analysis correct volume deficit
gravity Of the chemical and associated
Composition of aberrations in
urine electrolyte
concentrations
 Volume depletion

• Simplest form: pure water deficit (water

deficit without accompanying solute
deficit)
• Surgical patients: water and solute
deficit occur together (more often)
 Pure water deficit
(unable to regulate intake)

• Debilitated or comatose or increased

water loss from fever
• Tube feedings without adequate water
supplementation
• Diabetes insipidus
• Reflected by hypernatremia
 Pure water deficit
(associated findings)

• Plasma osmolality ↑
• Concentrated urine
• Low urine sodium (severe depletion)
 Pure water deficit
(clinical manifestation)

• Depress central nervous system:

lethargy, coma
• Muscle rigidity
• Tremors
• Spasticity
• seizures
 Pure water deficit
(Treatment)

• Enough water to restore the plasma sodium ( PNa )

concentration to normal
• △Na ＝ ( 140-PNa ) ×TBW
• △Na: the total milliequivalents of sodium in excess of
water
• Required water: △Na/140
• Ongoing obligatory water losses must be satisfied: due
to diabetes insipidus, fever etc.
 Volume and electrolyte depletion
causes

Gastrointestinal Other:
losses: Excessive diuretic therapy
nasogastric suction Adrenal insufficiency
Enteric fistulas Profuse sweating
Enterostomies Burns
diarrhea Body fluid sequestration
(trauma or surgery)
Volume and electrolyte depletion
(diagnosis)
history

Physical
signs

Records
diagnosis
Of intake
Clinical
And output
findings
 Volume and electrolyte depletion
(clinical findings)
• Urine Na+ concentration<10meq/L: aldosterone→ renal
tubule→ renal sodium conservation
• Hypertonic urine: >450-500mosm/kg
• Prerenal azotemia: BUN (blood urea nitrogen) ↑ ↑; serum
Cr (creatinine)↑; BUN/ Cr go as high as 20-25:1;
disproportionate rise (normal ratio:10:1)
• Acute tubular necrosis: BUN↑ Cr↑; ratio close to normal
Combined water-electrolyte deficits
Replacement
therapy

Calculate the Estimate

serum deficit volume deficit
from clinical
signs and
changes in
body weight
 Volume overload
ADH [ antidiuretic
Hormone] ← anesthesia
And surgical press

Circulatory
overload
Excessive fluid
Intake [immediate
Postoperative period]
Renal vasoconstriction
And increased
aldosterone
 Volume overload
[clinical manifestation]
Gallop rhythm Edema [ sacrum, extremities]
[cardiac failure]

Pulmonary artery clinical Jugular venous distension

And central venous
pressure↑
manifestation

Increased body weight Tachypnea [pulmonary edema]

 Volume overload
[management]

mild hyponatremia severe

Sodium restriction Water restriction diuretics

Specific electrolyte disorders

sodium
potassium

phosphorus

calcium
magnesium
 Specific electrolyte disorders
(Sodium )
• Hypernatremia: chiefly loss of water
• Hyponatremia: in patients with hyperlipidemia
or hyperproteinemia or hyperglycemia
• Acute, severe hyponatremia: occasionally
develops in patients undergoing elective
surgery. [excessive intravenous sodium-free
fluid administration]
 Specific electrolyte disorders
(Sodium )
• Most cases: treated by administering the calculated
sodium needs in isotonic solutions
• Use hypertonic sodium solutions: Severe
hyponatremia (PNa <120meq/L) produces mental
obtundation and seizures
• Rapid correction→ permanent brain damage
(osmotic demyelination syndrome)
• The increasing speed of serum Na+ not to exceed
10-12meq/L/h
 Specific electrolyte disorders
(potassium )

anabolism
Food K+ Intracellular K+

Small intestine Serum K+

catabolism
Stool, sweat
urine
Normal potassium metabolism
Serum potassium concentration [k+]
[k+]

pH of ECF Size of the

intracellular k+
pool
 Function of potassium
body cell plasma body cell plasma

acidosis hyperkalemia hypokalemia alkalosis

 Serum and digestive juice
electrolyte （ mmol/L ）
Na+ K+ Cl- HCO3-
serum 140 3.5-5.5 104 23-28
saliva 10-40 26 10-30 <10
Gastric juice 20 10-20 150 0

Pancreatic 140 5 40 110

juice
gall 140 5 100 40
Intestinal 140 5-15 60-110 30-80
juice
 Potassium excretion of kidney
Renal artery

Capillary vessel of
glomerulus

Renal corpuscle

proximal convoluted tubule

Renal vein

distal convoluted tubule

Disturbance of potassium metabolism
Disturbance of
potassium metabolism

Hypokalemia:
Hyperkalemia: Diuretics
Renal failure Adrenal steroid excess
Adrenal Renal tubular disorders
insufficiency (potassium wasting)
Deficient dietary potassium
intake
Alcoholic patients
Total parenteral nutrition with
inadequate potassium
replacement
 hyperkalemia
• Serum potassium concentration >5.5mol/L
• Treatable problem
• Fatal if undiagnosed
• Blood potassium levels must be closely
monitored in susceptible patients
 Hyperkalemia (clinical evidence)
• susceptible patients: severe trauma,
burns, crush injuries, renal insufficiency,
marked catabolism (other causes)
• Nausea and vomiting
• Colicky abdominal pain
• Diarrhea
• ECG changes (electrocardiographic)
 ECG changes of Hyperkalemia
(electrocardiographic)
ECG changes

Early changes Further elevation

peaking of T waves QRS like sine wave
Widening of QRS complex (portends imminent
Depression of ST segment cardiac standstill
ECG changes of Hyperkalemia
(electrocardiographic)
ECG changes of Hyperkalemia
(electrocardiographic)
 Assessment of hyperkalemia
1 2 3
Assess acidbase Determine the
⑴A true metabolic status rapidity to correct
abnormality?
the elevated
⑵ Elevated by serum potassium
hemolysis, marked
leukocytosis,
thrombocytosis
(platelet
>1million/L)
Emergency treatment of hyperkalemia
(five approaches)
1 Infusion: 50% GS +20u insulin (K+ ECF→ICF

2 Intravenous NaHCO3
solution
3 Calcium antagonize the tissue effects of K+

4 Cation exchange resin (orally or enema)

5 Sorbitol to induce
osmotic diarrhea
Hemodialysis for renal failure
 Hypokalemia
• Serum potassium concentration <3.5mol/L
• Causes:
renal wasting of potassium,
potassium deficiency,
inadequate dietary intake,
alcoholics,
elderly people with restricted diets
 Clinical manifestation
(neuromuscular function related)

• Decreased muscle contractility

• Decreased muscle cell potential
develop
• Paralysis of the muscles of respiration
(can cause death)
 Assess of hypokalemia
• Initial goal: identify the cause
• alkalosis→ hypolemia
• Renal losses → hypolemia (no acid-base imbalance, or
persists after alkalosis corrected)
• Renal potassium wasting (urine potassium excretion
>30meq/24h, and serum K+<3.5meq/l ):diuretic therapy,
alkalosis, increased aldosterone activity
• Total body deficit (urine potassium excretion
<30meq/24h)
 Treatment of hypokalemia
• Correct the cause
• Given orally (patient can eat), otherwise Intravenously
• Concentration in solution<40meq/L
• Moderate to severe (K+<3meq/L): administering rate:
20-30meq/L
• Mild (K+3-3.5meq/L): slowly to avoid hyperkalemia
• Use chloride salt of potassium often
• Refractary to replacement→ coexistent magnesium
deficiency?
 calcium
• Mediator of neuromuscular function and
cellular enzyme processes
• Dietary intake (1-3g/d), unabsorbed in feces
• Normal serum concentration: 4.2-5.2meq/L
• Maintained by: humoral factors, mainly
vitamin D, parathyroid hormone, calcitonin
 【 acid-base balance 】
blood buffer system
buffering acid buffering base
H2CO3 HCO3- + H+
H2PO4- HPO4- + H+
HHb Hb- + H+
HHbO2 HbO2- + H+
HPr Pr- + H+
HCO3- HCO3- 24 24 20
= = = =
H2CO3 0.03×PCO2 0.03×40 1.2 1
pH 7.35-
7.45
 【 maintaining of acid-base balance 】

pulmonary expiration

pH H2CO3 respiratory centre excited exaggerated and

fast expiration give off CO2 （ pH H2CO3 reverse

changes ）

renal regulation ： the most of all in acid-base balance ， get

rid of fixed acid and excessive base 。 （ see next picture ）
Renal tubule Blood vessel

Bicarbonate radical

exchange reabsorption

glutaminase

ketoglutarate

Acidification of urine Excretion of ammonia

renal regulation for acid-base balance

 Acid-base imbalance

metabolic acidosis decrease increase

metabolic
alkalosis
• （ HCO3-)
（ H2CO3)
•
respiratory increase decrease
respiratory
Acidosis alkalosis
 metabolic acidosis （ HCO3- )
pathogen

1 loss of alkaline matter ↑

2 acidoid comes into being ↑

3 renal insufficiency
dysfunction of secretion of H+ （ acidosis of
distal convoluted tubule ）
dysfunction of absorption of HCO3– （ acidosis of
proximal convoluted tubule ）
 Pathophysiology
① pulmonary expiration ：
HCO3- H2CO3relevant defused CO2 、 PCO2
stimulate respiratory centre 、 exaggerated and
fast expiration CO2 PCO2 HCO3-/H2CO3 close to 20/1
pH normal
compensated metabolic acidosis
② renal regulation ：
renal tubule generate H+ and NH3 H+ exchange with
Na+ and H+ combined with NH3 to be NH4 H+ exclude ,
NaHCO3 reabsorbed
 clinical manifestation
1 nerve system:
tired, giddy, somnolence, hypoesthesia, dottiness even
coma, tendon reflex weaken or disappear
2 respiratory system ：
deep and fast breath ， with ketone 。
3 cardiovascular system ：
rubeosis of face, increase of heart rate, low BP
4 other ：
accompanied with symptoms of severe water scarcity ，
decrease of myocardial contraction force and sensitivit
of peripheral blood vessels to catecholamine ， easy to
have arrythmia, acute renal failure and shock. Acidic
urine
Dignostic programe
1 History + classical clinical manifestation
2 Blood gas analysis
partly compensated ： pH, HCO3-, PCO2
decrease ( to some extent ）
uncompensated ： pH HCO3-decrease
obviously ， PCO2 normal
3 CO2-CP measuration ： obvious symptoms
<30%volume （ unconditional blood gas
analysis ）
4 Measuration of blood Na+ 、 K+ 、 Cl- helpful for
diagnosis
treatment
1 mild ： HCO3- >16-18mmol/L
eliminate etiologic factor, pulmonary and renal
regulation, acidosis can be corrected after
correction of dehydration without supplement
of base 。
2 severe ： HCO3- <10mmol/L
HCO3- （ mmol ） = HCO3-normal(mmol/L)-
HCO3-measured （ mmol/L ）
×body weight （ kg ） × 0.4
5%NaHCO3 diluted into 1.25% for application
*
 treatment
* 2-4h give half ， then give more after
carefully considering the actural
situation

•To supplement potassium when

correcting acidosis

* ionization of Ca++ increases in

acidosis ， it decreases after correction
++
Melabolic Alkalosis （ HCO3- )
pathogen
1 excess loss acidity gastric juice:
loss of H+ 、 Na+ Cl- and ECF ， HCO3-
reabsorption increase ； in renal tubule, K+
exchange with Na+, H+ exchange with Na+ ，
H+K+ excessive loss ， alkalosis and
hypokalemia.
2 excessive ingestion of base ：
take NaHCO3 for long time to treat digestive
ulcer
 pathogen

3 potassium depletion ：
exchange of K+ and Na+ ,H+ between
intracellular and extracellular, intracellular acidosis,
extracellular alkalosis
cells of distal convoluted tubule secret
excessive H+ ， HCO3- reabsorption increases,
abnormal acidity urine ；
4 pereira ：
for example: nicorol ( 速尿 )and urgent ( 利尿
酸 )excrete more Cl- than Na+ in urine ， Na+ and
HCO - reabsorption increases ， hypochloremic
Pathophysiology
1 pulmonary expiration ：
shallow and slow breath CO2 expiration
PCO2 HCO3-/H2CO3 close to 20/1 pH normal

2 renal regulation
renal tubule generate H+ and NH3 ; NaHCO3 reabsorbed
HCO3- exclude in urine
clinical manifestation
in general ,no symptoms
respiratory system ： slow and shallow breath ；
nerve system: phrenitis ( 谵妄 ), insanity ( 精神错
乱 ),hypersomia ( 嗜睡 ) etc. spiritual
abnormal ， even coma ；

diagnosis blood gas analysis can make sure

diagnosis and order of severity

partly compensated ： blood pH, HCO3- , PCO2↑

uncompensated ： blood pH, HCO3- increase
obviously ， PCO2 normal
 treatment
1 eliminate etiologic factor ：

loss of gastric juice→isotonic salt solution ，

correct hypochloremic alkalosis, supplement of
K+ to correct hypokalemia 。
2 Severe alkalosis ：
blood HCO3-40-50mmol/L,pH>7.65 ，
Equation for supplement of hydrochloric acid:
① supplement of hydrochloric acid (mmol)= HCO3-
measured (mmol/L)—HCO3- hope to reach
(mmol/L) ×body weight (kg) ×0.4
treatment

② supplement of hydrochloric acid = Cl-normal

(mmol/L) － Cl- measured (mmol/L) ×
volume of total body fluid （ 60% of body
weight ） ×0.2

* First 24h, give half ， not siutable to be

fast to correct alkalosis ， if lots of Cl- are
measured in urine, it means supplement
of Cl- enough
 Respiratory Acidosis
pathogen
ventilation of alveolus decrease, unable to completely
exclude CO2 generated in body ， blood PCO2 increases to
cause hypercapnia
① insufficiency pulmonary vnetilation ：
general anesthesia is too deep ,excess
narcotic( 镇静剂 ), cardiac arrest,
pneumothorax, tracheospasm, misemploy
of life-support machine etc.
② pulmonary diseases ， insufficiency pulmonary ventilation ：
pulmonary fibrosis, emphysema( 肺气肿 )etc
Pathophysiology

1 blood effective to buffer ：

PCO2 H2CO3 blood H2CO3cobined with

Na2PO4to be NaHPO3 and NaH2PO4 ， the
latter is excreted in urine ， H2CO3 HCO3-

2 renal regulation ：

Renal tubular epithelial cells generate H+ and

NH+3

H+ ,Na+ exchange and H+ combined with

NH+3to be NH+4 H+ excreted and NaHCO3
reabsorption , HCO3-/ H2CO3close to 20/1
again ， pH normal range 。
clinical manifestation
dyspnea, hypoventilation, malaise ；
tachypnea ( 气促 ), cyanosis ( 紫绀 ),
headache, chest distress ； BP low down
(severe), phrenitis( 谵妄 ), coma ；
diagnosis
history, clinical manifestation, blood gas
analysis
acute ： blood pH decrease obviously, PCO2
rise up, plasma HCO3- normal
chronic ： blood pH decrease not obviously,
PCO2 rise 、 plasmaHCO3- increase
treatment
radical method ： rapidly relieve obstruction of
respiratory tract ， improve pulmonary ventilation,
discharge the accumulate CO2 out from body
1 relieve obstruction of respiratory tract ：
for example: trachea cannula, life-support
machine 、 tracheotomy and so on
2 atelectasis ( 肺不张 ) ：
encourage deep inspiration, inflate lungs ， improve
ventilation, anti-infection ；
 treatmen
t
3 respiratory depression ： rescue breathing ( 人
工呼吸 ), stimulans of respiratory centre

4 severe respiratory acidosis ： give little

NaHCO3

5 oxygen supply ：

respiratory acidosis ， the most important is to

improve ventilation, not to merely supply
oxygen of high concentration, otherwise, it can
make reflex of sensor of respiratory centre to
Respiratory alkalosis

excessive ventilation of alveolus ( 肺泡 ) ， CO2

generated in body exsufflate too much ， blood
PaCO2 decrease ， lead to hypocapnia ， blood PH
increase
Clinical manifestation ：
tachypnea ， giddy ( 眩晕 ) ， numb of
hands, feet, and mouth
 Respiratory alkalosis

diagnosis ：
history ＋ clinical manifestation ， blood
gas analysis show: PH↑ ， PaCO2 and

HCO3- ↓hypocapnia ， blood PH ↑ 。

treatment ：
Use paper bag to cover nose and mouth
If necessary, block autonomous
respiration ， life-support machine
 control principle of water-electrolyte
metabolism and acid-base disorder
To prevent
1 Elementary daily requirement ：
water 2000-2500ml GS100-150g NaCl4-5g KCl3-4g
2 fever ： T increase 1℃ ， loss of hypotonic solution
through skin :3-5ml/kg
sweating ： moderate sweating: loss 500-
1000ml(NaCl3-4g)
great amount : loss 1000-1500ml
tracheotomy ： exhale evaporative water 2-3 times
more than normal ， about 800-1200ml
• treatment
• 1 、 estimate the situation of fluid and
electrolyte disorder specifically
• ① is there fluid and electrolyte
disorders ？
• ② is there water deficit ？
• ③ hypertonic dehydration or
hypotonic dehydration ？
• ④ is there acid-base imbalance ？
• ⑤ is there K+ 、 Ca++ deficit ？
• estimate amount and category of
fluid infusion specifically:
• ① supplement of intraday requirement
• ② supplement of extra loss of the other day
• （胃肠道等额外丧失、内在性失液、显性出汗
等）
• gastric juice ： 2:1 （ 5%GS : 5%GNS ）
• intestinal fluid ：
7:2:1 （ 5%GNS:5%GS:1.25NaHCO3 )
• with gall and pancreatic fluid ：
2:1 （ 5%GNS:1.25NaHCO3 ）
• pancreatic fluid ：
1:1( 5%GNS:1.25NaHCO3 ）
• * lose 1000mlgastrointestinal fluid ， give KCl
1-2g
•
③ supplement of the past loss ：
give half intraday ， give the other the
second, third day carefully considering he
actural situation

Normal standard of fluid and electrolyte

urine amount 40-50 ml/h
specific gravity 1.010-1.020
total chloride>4g/24h
•