FLUID AND ELECTROLYTE

MICHAEL ARITONANG, MD

Total Body Water (TBW)

Varies with age, gender, body habitus
60% body weight in males
50% body weight in females
80% body weight in infants
Less in obese: fat contains little water

Body Water Compartments

Intracellular water: 2/3 of TBW
Extracellular water: 1/3 TBW

- Extravascular water: 4/5 of extracellular water

- Intravascular water: 1/5 of extracellular water

Fluid and Electrolyte

Regulation
Volume Regulation
- Arginine-Vasopressin (ADH)
- Renin/angiotensin/aldosterone system
- Baroreceptors in carotid arteries and aorta
- ANP (Stretch receptors in atrium) and

juxtaglomerular apparatus

Fluid and Electrolyte Regulation

Plasma Osmolality Regulation
- Arginine-Vasopressin (ADH)
- Central and Peripheral osmoreceptors

Sodium Concentration Regulation

- Renin/angiotensin/aldosterone system
- Macula Densa of JG apparatus

Preoperative Evaluation of Fluid

Status
Factors to Assess:
- mental status
- intake and output
- blood pressure: supine and standing
- heart rate
- skin turgor
- urinary output
- serum electrolytes/osmolarity

Orthostatic Hypotension
Systolic blood pressure decrease of greater than

20mmHg from supine to standing

Indicates fluid deficit of 6-8% body weight
- Heart rate should increase as a compensatory
measure
- If no increase in heart rate, may indicate autonomic
dysfunction or antihypertensive drug therapy

Perioperative Fluid
Requirements
The following factors must be taken into account:
Maintenance fluid requirements
NPO and other deficits: NG suction, bowel prep
Third space losses
Replacement of blood loss
Special additional losses

Maintenance Fluid
Requirements

Insensible losses such as evaporation of water

from respiratory tract, sweat, feces, urinary

excretion. Occurs continually.
Adults: approximately 1.5 ml/kg/hr
4-2-1 Rule
- 4 ml/kg/hr for the first 10 kg of body weight
- 2 ml/kg/hr for the second 10 kg body weight
- 1 ml/kg/hr subsequent kg body weight
- Extra fluid for fever, tracheotomy, denuded
surfaces

NPO and other deficits

NPO deficit = number of hours NPO x

maintenance fluid requirement.

Bowel prep may result in up to 1 L fluid loss.
Measurable fluid losses, e.g. NG suctioning,
vomiting, ostomy output.

Third Space Losses

Isotonic transfer of ECF from functional body

fluid compartments to non-functional

compartments.
Depends on location and duration of surgical
procedure, amount of tissue trauma, ambient
temperature, room ventilation.

Replacing Third Space Losses

Superficial surgical trauma: 1-2 ml/kg/hr
Minimal Surgical Trauma: 4-6 ml/kg/hr

- head and neck, hernia, knee surgery

Moderate Surgical Trauma: 6-8 ml/kg/hr
- hysterectomy, chest surgery
Severe surgical trauma: 8-12 ml/kg/hr (or
more)
- AAA repair, nehprectomy

Blood Loss
Replace 3 cc of crystalloid solution per cc of

blood loss (crystalloid solutions leave the

intravascular space)
When using blood products or colloids replace
blood loss volume per volume

Allowable blood loss

1. Estimate blood volume
2. Estimate the red blood cell volume (RBCV) at

the preoperative hematocrit (RBCVpreop).

3. Estimate RBCV at a hematocrit of 30%

(RBCV30%), assuming normal blood volume is

maintained.
4. Calculate the red cell volume lost when the
hematocrit is 30%; RBCVlost = RBCVpreop RBCV30%.
5. Allowable blood loss = RBCVlost x 3.

Example
An 85-kg woman has a preoperative hematocrit

of 35%. How much blood loss will decrease her

hematocrit to 30%?
Estimated blood volume = 65 mL/kg x 85 kg =
5525 mL.
RBCV35% = 5525 x 35% = 1934 mL.
RBCV30% = 5525 x 30% = 1658 mL.
Red cell loss at 30% = 1934 1658 = 276 mL.
Allowable blood loss = 3 x 276 mL = 828 mL.

Other factors
Ongoing fluid losses from other sites:

- gastric drainage
- ostomy output
- diarrhea
Replace volume per volume with crystalloid
solutions

Intravenous Fluids:
Conventional Crystalloids
Colloids
Hypertonic Solutions
Blood/blood products and blood substitutes

Crystalloids
Combination of water and electrolytes

- Balanced salt solution: electrolyte composition

and osmolality similar to plasma; example:
lactated Ringers & Normosol.
- Hypotonic salt solution: electrolyte composition
lower than that of plasma; example: D5W.

Colloids
Fluids containing molecules sufficiently large

enough to prevent transfer across capillary

membranes.
Solutions stay in the space into which they
are infused.
Examples: hetastarch , albumin, dextran.

Advantage of colloids vs crystalloid

iv
fluids

Colloid
smaller infused volume
prolonged increased in plasma volume
less peripheral edema
Crystalloid
lowest cost
greater urinary flow
interstitial fluid replacement

Disadvantages
Colloid

greater cost
coagulopahty (dextran > HES)
decrease GFR
greater duration of excessive volume expansion
Crystalloid
transient increased in intravascular volume
transient hemodynamic improvement
pheripheral edema and pulmonary edema

Hypertonic Solutions
Fluids containing sodium concentrations

greater than normal saline.

Available in 1.8%, 3%, 5%, 7.5%, 10%
solutions.
Hyperosmolarity creates a gradient that
draws water out of cells; therefore, cellular
dehydration is a potential problem.

Composition

Clinical Evaluation of Fluid

Replacement
1. Urine Output: at least 0.5- 1.0 ml/kg/hr
2. Vital Signs: BP and HR normal (How is the
patient doing?)
3. Physical Assessment: Skin and mucous
membranes no dry; no thirst in an awake patient
4. Invasive monitoring; CVP may be used as a
guide
5. Laboratory tests: periodic monitoring of
hemoglobin and hematocrit

Electrolyte Balance

Electrolytes are salts, acids, and bases, but

electrolyte balance usually refers only to salt
balance
Salts are important for:
Neuromuscular excitability
Secretory activity
Membrane permeability
Controlling fluid movements
Salts enter the body by ingestion and are lost
via perspiration, feces, and urine

Sodium in Fluid and Electrolyte

Balance

Sodium holds a central position in fluid and

electrolyte balance
Sodium salts:
Account for 90-95% of all solutes in the ECF
Contribute 280 mOsm of the total 300 mOsm
ECF solute concentration
Sodium is the single most abundant cation in the
ECF
Sodium is the only cation exerting significant
osmotic pressure

Sodium in Fluid and Electrolyte

Balance

The role of sodium in controlling ECF volume and

water distribution in the body is a result of:

Sodium being the only cation to exert
significant osmotic pressure
Sodium ions leaking into cells and being
pumped out against their electrochemical
gradient
Sodium concentration in the ECF normally
remains stable

Sodium in Fluid and Electrolyte

Balance
Changes in plasma sodium levels affect:
Plasma volume, blood pressure
ICF and interstitial fluid volumes

Renal acid-base control mechanisms are coupled

to sodium ion transport

Regulation of Sodium Balance:

Aldosterone
Sodium reabsorption
65% of sodium in filtrate is reabsorbed in the

proximal tubules
25% is reclaimed in the loops of Henle
When aldosterone levels are high, all remaining
Na+ is actively reabsorbed
Water follows sodium if tubule permeability has
been increased with ADH

Regulation of Sodium Balance:

Aldosterone
The renin-angiotensin mechanism triggers the release

of aldosterone
This is mediated by the juxtaglomerular apparatus,
which releases renin in response to:
Sympathetic nervous system stimulation
Decreased filtrate osmolality
Decreased stretch (due to decreased blood
pressure)
Renin catalyzes the production of angiotensin II,
which prompts aldosterone release

Regulation of Sodium Balance:

Aldosterone

Adrenal cortical cells are directly stimulated

to release aldosterone by elevated K+ levels

in the ECF
Aldosterone brings about its effects
(diminished urine output and increased
blood volume) slowly

Regulation of Sodium Balance: Aldosterone

Figure 26.8

Cardiovascular System
Baroreceptors
Baroreceptors alert the brain of increases in
blood volume (hence increased blood
pressure)
Sympathetic nervous system impulses to
the kidneys decline
Afferent arterioles dilate
Glomerular filtration rate rises
Sodium and water output increase

Cardiovascular System
Baroreceptors

This phenomenon, called pressure diuresis,

decreases blood pressure

Drops in systemic blood pressure lead to
opposite actions and systemic blood pressure
increases
Since sodium ion concentration determines fluid
volume, baroreceptors can be viewed as
sodium receptors

Maintenance of Blood Pressure Homeostasis

Figure 26.9

Atrial Natriuretic Peptide

Reduces blood pressure and blood volume by
(ANP)
inhibiting:
Events that promote vasoconstriction
Na+ and water retention
Is released in the heart atria as a response to
stretch (elevated blood pressure)
Has potent diuretic and natriuretic effects
Promotes excretion of sodium and water
Inhibits angiotensin II production

Mechanisms and Consequences of ANP

Release

Figure 26.10

Influence of Other Hormones on

Sodium Balance
Estrogens:
Enhance NaCl reabsorption by renal tubules
May cause water retention during menstrual

cycles
Are responsible for edema during
pregnancy

Influence of Other Hormones on

Sodium Balance
Progesterone:
Decreases sodium reabsorption
Acts as a diuretic, promoting sodium and

water loss
Glucocorticoids enhance reabsorption of
sodium and promote edema

Regulation of Potassium
Balance
Relative ICF-ECF potassium ion concentration
affects a cells resting membrane potential
Excessive ECF potassium decreases
membrane potential
Too little K+ causes hyperpolarization and
nonresponsiveness

Regulation of Potassium
Balance
Hyperkalemia and hypokalemia can:
Disrupt electrical conduction in the heart
Lead to sudden death

Hydrogen ions shift in and out of cells

Leads to corresponding shifts in potassium in

the opposite direction

Interferes with activity of excitable cells

Regulatory Site: Cortical

Collecting Ducts

Less than 15% of filtered K+ is lost to urine

regardless of need
K+ balance is controlled in the cortical collecting
ducts by changing the amount of potassium
secreted into filtrate
Excessive K+ is excreted over basal levels by
cortical collecting ducts
When K+ levels are low, the amount of secretion
and excretion is kept to a minimum
Type A intercalated cells can reabsorb some K+
left in the filtrate

Influence of Plasma Potassium

Concentration
High K+ content of ECF favors principal cells to

secrete K+
Low K+ or accelerated K+ loss depresses its
secretion by the collecting ducts

Influence of Aldosterone
Aldosterone stimulates potassium ion secretion

by principal cells
In cortical collecting ducts, for each Na+
reabsorbed, a K+ is secreted
Increased K+ in the ECF around the adrenal
cortex causes:
Release of aldosterone
Potassium secretion
Potassium controls its own ECF concentration via
feedback regulation of aldosterone release

Regulation of Calcium
Ionic calcium in ECF is important for:
Blood clotting
Cell membrane permeability
Secretory behavior

Hypocalcemia:
Increases excitability
Causes muscle tetany

Regulation of Calcium
Hypercalcemia:
Inhibits neurons and muscle cells
May cause heart arrhythmias

Calcium balance is controlled by parathyroid

hormone (PTH) and calcitonin

Regulation of Calcium and

Phosphate

PTH promotes increase in calcium levels by

targeting:
Bones PTH activates osteoclasts to break
down bone matrix
Small intestine PTH enhances intestinal
absorption of calcium
Kidneys PTH enhances calcium reabsorption
and decreases phosphate reabsorption
Calcium reabsorption and phosphate excretion
go hand in hand

Regulation of Calcium and

Phosphate
Filtered phosphate is actively reabsorbed in the

proximal tubules
In the absence of PTH, phosphate reabsorption is
regulated by its transport maximum and excesses
are excreted in urine
High or normal ECF calcium levels inhibit PTH
secretion
Release of calcium from bone is inhibited
Larger amounts of calcium are lost in feces and
urine
More phosphate is retained

Influence of Calcitonin
Released in response to rising blood calcium

levels
Calcitonin is a PTH antagonist, but its
contribution to calcium and phosphate
homeostasis is minor to negligible

Hypernatremia
Na > 145

Major causes
Impaired thirst obtunded , anesthetized px and
infants
Solute diuresis osmotic diuresis
Excessive water losses Renal, Extra renal
Decrease urinary concentrating ability (DI)
urinary osmolality <150mOsm/kg,
hypertonicity and polyuria is diagnostic of DI

Hypernatremia
Clinical manifestation

Restlessness

Lethargy

hyperreflexia

seizure

coma
Acute severe hypernatrimia ( acute increase
from 146-170mEq/L) cause neurological
damageat 24 hours : Central Pontine Myelinosis.

Hypernatremia
Treatment
Aim restoring plasma osmolality to normal
Water deficit should be corrected over 48 hours

Acute treatment
Sodium depletion (hypovolemia)

hypovolemia correction (0.9% saline)

hypernatremia correction (hypotonic fluids)
Sodium overload (hypervolemia)

Enhance sodium remocal ( loop diuretics,

dialysis)
Replace water deficit (hypotonic fluids)

Acute treatment Cont..

Normal Total body sodium (euvolemia)

replace water dificit (hypotonic fluids)

control Diabetic Insipidus
1. Central DI:
DDAVP,10-20mcg intranasally; 2-4mcg SC
2. Nephrogenic DI:
Restrict Na and water intake
Thiazide diurectics

Hypernatremia
Hypernatremia

Water & Na loss

Water Loss

Increased Na Content

Replace isotonic loss

Replace water deficit

Loop diuretic

Raplace water deficit

Replace ani water def

Hypernatremia
Anesthetic Considerations
Increases MAC
Hypovolemia accentuates any vasodilatation or

cardiac depression from anesthetic agents

Elective surgery should be postponed in patients
with Na > 150 mEq/L

Hyponatremia
Na+ < 135 mEq/L
Fluid losses resulting in hyponatremia may be

renal and extra renal

Renal related to thiazide diuretic
Extra renal are typically gastrointestinal
SIADH

SIADH
Diagnostic Criteria For Syndrome of Inappropriated

AntiDiuretic Hormone Secretion

1. Hyponatremia with appropriately low plasma
omolality
2. Urinary osmolality > Plasma Osmolality
3. Renal Na excretion > 20mmol/L
4. Absence of hypotension, hypovolemia and
edematous states
5. Normal reanal and Adrenal function
6. Absence of drugs that directly influence renal
water and Na

Algorithm for the diagnosis of the cause of the hyponatremia

Hyponatremia
Anesthesia Consideration
Plasma sodium concentrations should be

corected above 130 mEq/L for elective procedure

Lower concentration may result in significant
cerebral edema ( mac, post op agitation,
confusion, or somnolence)

Hypokalemia
Plasma K < 3.5 mEq/L
Can occur as result

an intercompartemental shift of K
increase potassium loss
inadequate potassium intake

Causes of Renal Potassium

Drugs
Bicarbonaturia
Loss
Diuretucs
Distal renal Tubular Acidosis
Thiazide Diuretics Magnesium deficiency
Loop Diuretics Other less common causes
Osmotic Diuretics
Cisplatin
Antibiotics
Carbonic anhydrase inhibitors
Penicillins
Leukemia
Hormones
Intrinsic renal defect
Aldosterone
Barter syndrome
Glucocorticoids
Gitelman syndrome

Hypokalemia
Effects
Cardiovascular
Neuromuscular
Renal
Hormonal
Metabolic

Hypokalemia
Treatment depends on presence and severity of

any associated organ dysfungtion

Oral replacement with potassium chloride sol is
generally safest ( 60-80 mEq/dl)
Peripheral IV replacement should not exceed 8
mEq/hours
Avoid Dextrose-containing sol

Hypokalemia
Anesthetic Consideration
Chronic mild hypokalemia (3-3.5mEq/L) wo ECG

changes not increase anesthetic risk

Dosages of neuromuscular blocking agents
should therefore be reduced 25-50%

Hyperkalemia
Plasma K exceeds 5.5 mEq/L
Can occurs

an intercompartemental shift of pottasium

decreased urinary excretion of potassium
an increase potassium intake

Hyperkalemia
Effect on skeletal and cardiac muscle
Skeletal muscle weakness sen if plasma K is

greater than 8 mEq/L

ECG changes

Hyperkalemia
Treatment
Hyperkalemia exceeding 6 mEq/L should always

be treated
Severe hyperkalemia treatment
Reverse membrane effects
Transfer extracellular Potassium into cells
Remove Potassium from body

Hyperkalemia
Anesthesia consideration
Elective surgery should not be undertaking in

patients with hyperkalemia

Succinylcholine is contraindecated

Hypercalcemia
Causes of hypercalcemia
Hyperparathyroidism
Malignancy
Excessive vit D Intake
Pagets disease
Granulomatous disorders
Chronic immobilization
Milk-alkali syndrome
Adrenal insufficiency
Drug induced

Hypercalcemia
Clinical Manifestation
Anorexi,Nausea,Vomiting,Weakness,Polyuria,ata

xia,Letargia,Confusion
HPN, Arrhythmias, Heart block, and Cardiac
Arrest
ECG signs ST segment and shortened QT
interval
Increases cardiac sensitivity to digitalis

Hypercalcemia
Treatment
Rehydration followed by a brisk diuresis ( urinary

output 200-300 ml/hour) with administration of iv

saline infusion and loop diuretic to accelerate
calcium excretion.
Biphosphonate, 1st line drugs for management of
hypercalcemia due to osteoclastic bone resorption.
Calcitonin
Hydrocortisone

Hypercalcemia
Anesthetic consideration
Hypercalcemia is a medical emergency
Responses to anesthetic agent are not

predictable

Hypocalcemia
Causes
Hypoparathyroidism
Pseudohypoparathyroidism
Vitamin D deficiency
Hyperphosphathemia
Precipitation of ca
Chelation of ca

Hypocalcemia
Clinical manifestation
Paresthesis, confusion, laryngeal

stridor,carpopedal spasm, masseter spasm and

seizures
Biliary colic, broncho spasm
Cardiac irritability

Hypocalcemia
Treatment

Administer Calcium
Iv: 10 mL 10% calcium gluconate over 10min, followed by
elemental calcium
oral: 500-100mg elemental calcium q6hr
Administer vitamin D
Ergocalciferol, 1,200mcg/day
Dyhydrotachysterol,200-400mcg/day
1.25 dihydroxycholecalciferol, 0,25-1.0 mcg/day

Hypocalcemia
Anesthetic consideration
Should be corrected preoperatively
Avoid alkalosis to prevent further decreases in

Ca
IV ca may necessary following rapid transfusion
of citrated blood products or large volumes
albumin solution
Potentiation of negative effects of barbiturates
and volatile anesthetic
Responses to neuromuscular blocking agents
are inconsistent

Hyperphosphatemia
Secondary effect on plasma Ca
Though to lower plasma Ca by precipitation and

deposition of ca phosphate in bone and soft

tissue
Treatment phosphate-binding antacids such as
aluminiumhydroxide or aluminium carbonat

Hypophosphatemia
Result of either a negative phosphorous balance

or cellular uptake of extracelular

Clinical manifestations severe
hypophosphatemia often associated with
widespread organ dysfunction
Treatment- Potassium or sodium phosphate ( 2-5
mg of elemental phosphourous per kilogram, or
10- 45 mmol slowly over 6 12 hours)
Anesthetic consideration neuromuscular
function must be monitored when neuromuscular
blocking agen are giving

Hypermagnesemia
Clinical Manifestation neurologic ,

neuromuscular manifestation
Treatment IV calcium
Anesthesia consideration
Dosages of neuromuscular blocking agents
should be reduced

Hypomagnesemia
Asymptomatic
Associated with both hypocalcemia and

hypokalemia
Cardiac manifestation
Treatment magnesium sulfate

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