Fluids and Electrolytes (Part 1) PUBERTY: males and females develop different levels
Dr. R. Mendoza due to differences in fat/muscle content
September 2, 2013
Group 2big
REASONS WHY CHILDREN AND ADULTS HAVE
DIFFERENT FLUID REQUIREMENTS
1. Higher metabolic rate
- daily water turnover is 15% of total body
water (TBW)
2. Larger skin surface area in relation to body size
- 2-3x of adult
3. Prone to greater loss of fluid
4. Immaturity of the kidney
- Inability to concentrate urine
WATER
TBW Major Components:
1. Intracellular Fluid (ICF)
2. Extracellular Fluid (ECF)
a. Interstitial fluid
b. Plasma
Fig 1. Body weight-water ratios
BIRTH: total body water is 75-80% of total body wt
(ECF > ICF), and infants appear edematous. Fluid loss
due to postnatal diuresis and increased growth of
cells occurs during the 1st 24 hours and continues for
1-2 weeks. ICF will then be greater than ECF.
Physiologic weight loss should not exceed 10%; infant
will regain lost weight by three weeks.
PRE-TERM: have higher percentage of total body
water, around 90%.
1ST YEAR: TBW decreases to approximately 60% of
body weight, with ICF and ECF levels approximating
that of adults.
10-15% difference
OBESE: decreased body water, difficult to manage
fluid disturbances, poor prognosis.
e.g. dengue fever capillary permeability, loss
of albumin resulting to fluid shift from
intravascular to 3rd spaces.
COMPARTMENTS OF BODY WATER
Intracellular 30-40%
Extracellular 20-25%
Interstitial fluid 15%
Plasma 5%;
up to 10% in newborn infants (have 50-60% Hct)
Fig 2. Total body water and distribution
MOVEMENT OF BODY FLUIDS
Kun diin ang mas lapuyot, didto magkadto ang tubig
1. Hydrostatic Pressure -
2. Diffusion- movement of particles down a
concentration gradient (higher to lower
concentration)
3. Osmosis- due to protein and sodium concentration;
diffusion of water across a selectively permeable
membrane.
4. Active transport- movement of particles up a
concentration gradient; requires energy;
exemplified by Na-K ATPase pump
ECF HOMEOSTASIS IS MAINTAINED BY:
1. Hydrostatic Pressure (Blood Pressure)
Movement is from higher to lower pressure
- Pumping action of the heart
- More prominent in arterial end
- Drives fluid out of the intravascular space
- Affected by:
a. diameter of blood vessel involved
b. volume of extracellular fluids
 a. Plasma
2. Oncotic Pressure (Osmotic pressure) Dehydration GI losses, vomiting, renal losses
- Primarily due to albumin (cannot cross the 5% = moderate dehydration
intravascular membrane because of its high Anemia very diluted plasma volume
molecular weight; establishes a gradient Polycythemia very concentrated blood
between the intravascular and interstitial spaces) Heart failure venous insufficiency causes
- Draws water into the intravascular space damming and subsequent blood volume (BV)
- Depends on: Abnormal plasma osmolality
a. level of non-diffusing proteins in plasma and Hypoalbuminemia
interstitial fluids. b. Interstitial
b. concentration of electrolytes, especially Na+ Heart failure
Higher solute solutions draw water. Liver failure
Nephrotic syndrome

EDEMA
- accumulation of fluid in the interstitial spaces

Fig 3. Capillary fluid exchange
*At the arterial end, there is high hydrostatic pressure,
driving water out of the capillaries and into the
interstitial space. At the venous end, there is an
increase in oncotic pressure due to higher albumin to
water ratio, so water is drawn back into the
intravascular space.
*Usually there is a net movement of fluid out of the
intravascular space; excess fluid at venous end is
absorbed by lymphatics.
*Tissue perfusion is maintained by ECF homeostasis:
intravascular volume = blood flow to organs =
oxygen delivery 2. Anions
From past notes:
HYDROSTATIC PRESSURE INCREASES DUE TO:
a. Venous obstruction
Thrombophlebitis (inflammation of veins) ELECTROLYTE COMPOSITION
Hepatic obstruction
Tight clothing on extremities
Prolonged standing
b. Salt or water retention
Congestive heart failure
Renal failure
Causes of edema:
1. Increased hydrostatic pressure
2. Lowered plasma osmotic pressure liver failure
3. Increased capillary membrane permeability
Almost always due to a disease
dengue hemorrhagic fever (fluids and albumin leak
out of intravascular space)
4. Lymphatic channel obstruction tumors, masses
SOLUTES
- dissolved particles, usually in water (universal
solvent)
ELECTROLYTES (charged particles)
1. Cations
- positively charged particles
- Na+, K+, Ca2+, H+
- move against the concentration gradient, require
Na+-K+-ATPase pump
- negatively charged particles
- Cl-, HCO3-, PO43-
- diffusion

FACTORS AFFECTING THE EXTRACELLULAR

FLUID
 PLASMA INTRACELLULAR
Cations Cations OSMOLALITY
Na+ 140 K+ 140 kun ano kalapuyot imu dugo
+
K 4 Na+ 13 Osmolality = osmolarity
Ca++ 2.5 Mg++ 7
Mg++ 1.1 I. PLASMA OSMOLALITY
concentration of solute particles in plasma
Anions Anions - Na+, blood glucose, urea nitrogen
Cl- 104 PO3- 107 2x (Na+) + (glucose) /18 + (BUN)/2.8
HCO3- 24 Protein 40 Normal plasma osmolality = 285-295 mOsm/kg H 2O
Protein 14 HCO3- 10 Sodium is the most important solute involved in
Other 6 Cl- 3 determining plasma osmolality.
PO3- 2 Sodium and glucose are the only effective osmoles.
Urea is equal intracellularly and extracellularly
Electrolytes in the different compartments are (ineffective osmole) because it readily crosses cell
electrically neutral. membranes.
Difference in ECF & ICF cation composition is due to only significant in patients with uremia or are
the Na+K+ATPase pump. undergoing hemodialysis, where shift is rapid
Difference in ECF & ICF anion composition is due to Diabetic ketoacidosis - hyperglycemia
the presence of intracellular molecules that do not
cross the cell membrane. II.EFFECTIVE OSMOLALITY (TONICITY)
2x (Na+) + (glucose)/18
IMPORTANT NOTES: Determines the osmotic force mediating the shift of
- If valence is 1: water between the ECF and ICF
meq = mmol water moves to areas with greater concentrate levels.
- If valence is > 1:
meq= mmol x valence MEASURED OSMOLALITY CALCULATED OSMOLALITY
- meq = mg/atomic wt x valence Osmolal gap (>10 mOsm/kg)
- mg = meq x atomic wt/valence 1. unmeasured osmoles
Atomic wts: - occurs in poisoning
Ca 40 - ethanol, ethylene glycol, methanol, mannitol
K 39 2. pseudohyponatremia
Na 23 - seen in those with increased cholesterol levels
Example: - increased lipid and protein in the plasma
Convert 2000 mg of Na to meq
meq = 2000/23 x 1 REGULATION OF OSMOLALITY
= 87 meq Na Dependent on water balance (intake = losses)
Increased osmolality leads to conservation of water
NON ELECTROLYTES (uncharged particles) A change of 1% in osmolality is detected by the
- proteins, urea, glucose, O2, CO2 hypothalamus.
- present in the interstitial fluid, plasma and ADH stimulates aquaporin (water channels) in the
intracellular fluid. collecting ducts of the kidney, permitting
- If the valence of the electrolyte is 1, mmol = reabsorption of water concentrated urine
mmEq. Baroreceptors in the hypothalamus recognize
decrease in fluid volume ( osmotic pressure)
BODY FLUIDS ARE: o sweating, salivation, dry mouth, BV
- Electrically neutral activate renin-angiotensin pathway stimulate
- Osmotically maintained (specific number of particles thirst centers water intake
per volume of fluid) Restoration of intravascular volume always takes
- If the osmolality in the extracellular fluid increases, precedence over the control of osmolality, because
water from the intracellular space will go out to
maintain equilibrium.
 intravascular volume is very important in tissue
perfusion.
Correct fluid deficits before correcting electrolyte
imbalances.

Fig 4. Mechanisms of osmoreception and osmoregulation

Fig 5. Renin-Angiotensin-Aldosterone System
Thirst reflex triggered by:
decreased salivation & dry mouth
increased osmotic pressure
decreased blood volume

RESULT:
Increased water consumption
Increased water conservation (activation of ADH)
Increased water in body, increased volume
Decreased Na+ concentration

REGULATION OF VOLUME

Renin-Angiotensin System
- important regulator of renal Na+ excretion Fig 6. Nephron structure

Na+ balance is the main regulator : where Na+ goes,
water follows
Kidney determines sodium balance alters the
percentage of filtered Na+ reabsorbed in the nephron
depending on the volume status of the patient
Sodium reabsorption can occur in all areas of the
kidney.
Majority (65%) of sodium is reabsorbed in the
proximal collecting tubule (PCT) and distal loop of
Henle. If there is a need to reabsorb more sodium,
the distal collecting tubule (DCT) and collecting ducts
also help (regulated by aldosterone).
Regulation of Volume
1. Volume expansion
- Inhibition of Na+ reabsorption in collecting ducts
2. Volume depletion
- Renal retention of Na+
Effective volume is the volume in the intravascular
space that is sensed by the receptors in the body.
If there is heart failure, there is volume overload. A
lot of fluid is in the intravascular areas but there is
very low effective volume; very little goes to kidney,
most stay in the interstitial space.
Renin is produced in the juxtaglomerular apparatus.
Angiotensin II has a vasoconstrictor effect BP
FLUID HOMEOSTASIS MAINTAINED BY
1. Ion Transport
2. Water Movement
3. Kidney Function Blood vessel

Body fluids are:

- Electrically neutral
- Osmotically maintained (specific number of
particles per volume of fluid)

OSMOLALITY DISTURBANCES
ECF H2 O Na+ < 135 mmol/L
HYPERTONIC STATE (PV)

Blood vessel

ICF
Cell

Fig 8. Movement of fluids in hypotonic state.

In hypotonic state, ICF has higher sodium

ECF + concentration; fluid enters the cell, leading to cell
Na > 145 mmol/L
(PV) swelling.
Most dreaded complication increased ICP leading
to brainstem herniation.
Also corrected gradually though not as slow as
H2 hypertonia.
O Cell ISOTONIC STATE
ICF

Fig7. Movement of fluid in hypertonic states. ECF (PV) H2 O Na+ = 135-145mmol/L

In the hypertonic state, ECF has higher sodium Blood vessel

concentration; fluid leaves the cell, leading to cell
shrinkage.
Most dreaded complication brain hemorrhage
ECF (IF)
(seizure) Na+ = 135- H2O Cell
In correcting, lower Na+ gradually. 145mmol/L ICF
HYPOTONIC STATE
Fig 9. Movement of fluids in isotonic states.

CLINICAL FEATURES OF Na+/OSMOLALITY

DISTURBANCE
Isotonic Hypotonic Hypertonic
SKIN - Cold & dry - Cold & clammy - Warm, velvety - Extrarenal losses (GI, sweat, burn, 3rd space loss)
- Poor - Very poor doughy - Renal losses:
elasticity & elasticity & - Normal to slightly o Thiazide/loop diuretics
turgor turgor poor elasticity o Osmotic diuresis
LIPS & - Dry - Clammy or - Parched, with o Lack of aldosterone
TONGUE moist complaints of Euvolemic Hyponatremia
- Presence of extreme thirst - SIADH
hypersalivation
- Desmopressin acetate
CNS - Lethargic - Comatose; - Lethargic or
- Glucocorticoid deficiency
occasionally hyperirritable,
- Hypothyroidism
with seizures, muscle
generalized
- Water intoxication
tone & deep
convulsions tendon reflexes Hypervolemic Hyponatremia
(DTR) - Congestive heart failure
VITAL - Normal to - Very low - Febrile - Cirrhosis
SIGNS low temp temperature temperature - Nephrotic syndrome
- Normal to - BP in shock - Normal BP - Renal failure
low BP - Thready pulse - Normal to slightly - Sepsis with capillary leak
- Rapid PR increased PR - Hypoalbuminemia

In hypertonic state, normal BP is possible: ICF shifts Severe hyponatremia

to intravascular spaces (volume depletion correction - Serum Na+ < 120 mEq/L
as compensatory mechanism). - Patients are often symptomatic
Check if patient is feeling warm or thirsty, if present o Convulsions, shock, lethargy (seizures)
may have hypertonia. - Treatment: NaCl: 2 mEq/ml
Most common cause of hypotonia in children is
gastroenteritis. Hypernatremia is rare. (Del Mundo) Calculating amount of Na+ needed
N = (desired Na+ conc - actual Na+) x weight in kg X 0.6
Ex. Actual Na+ = 112 mEq
Weight = 10 kg
Desired Na+ = 125mEq
+
ELECTROLYTES Na needed = (125-112) x 10 x 0.6 = 78 mEq of NaCl

COMPOSITION OF DIFFERENT INTRAVENOUS FLUIDS

Sodium
HCO3
Main cation of ECF (135-145 mEq/L) Solution
Na+ K+ Cl- Lactate Acetate Ca++ Mg++
Low in ICF (less than 3%) Lactated Ringers 130 4 109 28 - 1.5 -
Pairs with Cl-, HCO3- to neutralize charge Isotonic Saline (NSS) 154 - 154 - - - -
Na+K+ATPase pump maintains sodium concentration 0.3% NaCl 51 - 51 - - - -
Most important ion in regulating water balance 0.45% NaCl 77 - 77 - - - -
Important in nerve and muscle function Ionosol MB (IMB) 25 20 22 23 - - 1.5
Normosol M (NM) 40 13 40 - 16 - 1.5
Regulation of Sodium Normosol R (NR) 140 5 98 - 27 - 1.5
Absorbed throughout the GIT
Kidney is the principal site of Na+ excretion D5 0.45% NaCl is not available in the Philippines. To
Renal tubule reabsorption affected by hormones: prepare D50.45%: 500 ml of NSS + 500 ml D5Water.
- Aldosterone Recheck if you have corrected the deficit. You still
- Renin/angiotensin have to account for the maintenance which is 2-3
mEq/kg.
Causes of Hyponatremia:
Hyperosmolality HYPERNATREMIA
- Hyperglycemia, mannitol - Patients are irritable, restless, weak and lethargic;
Hypovolemic Natremia high-pitched cry, brain hemorrhage, seizure
 - Deficit, maintenance and replacement therapy is - dried fruits (prunes), fruits (banana,
given over a period of 48 hours not rapidly!! cantaloupe, grapefruit, orange, apricots,
- Fluid of choice should contain a Na+ concentration avocado)
of 25 mEq/L (maintenance IV fluid) - vegetables (spinach, broccoli, green beans)
nuts
CAUSES OF HYPERNATREMIA: - milk, meat
Excessive Sodium - coffee & cola
- Improperly mixed formula - salt substitutes
- Excess sodium bicarbonate
- Ingestion of seawater CAUSES OF HYPOKALEMIA:
- Intentional/unintentional salt poisoning Spurious artificial decrease in K+ levels
- IV hypertonic saline Transcellular shifts
- Hyperaldosteronism Decreased intake
Water Deficit Extrarenal causes:
- Nephrogenic diabetes insipidus - Diarrhea
- Central diabetes insipidus - Laxatives
- Increased insensible water loss - Sweating
- Inadequate intake Renal losses:
Water and Sodium Deficits - Distal renal tubular acidosis
- GI losses (diarrhea, vomiting, osmotic cathartics) - Tubular toxins
- Cutaneous losses (burns, excessive sweating) - Diabetic ketoacidosis
- Renal losses - Low urine chloride
o Osmotic diuretics
o Diabetes mellitus ELECTROCARDIOGRAPHIC (ECG) Changes in
o Chronic renal disease Hypokalemia:
o Acute tubular necrosis Flattened T wave
o Postobstructive diuresis Depressed ST segment
Appearance of a U wave
If a patient arrives at the ER in shock with suspected
hypernatremic dehydration, fluid of choice is NSS and
LR, regardless of the osmolality disturbance.

POTASSIUM
Mainly found in muscles
Plasma concentration is not always reflective of the
total body content (if you are acidotic, H+ goes into
the cell in exchange for potassium) Fig 10. ECG changes in hypokalemia.
Na+-K+-ATPase pump maintains K+ concentration
Exchanges with H ions to maintain acid-base balance Skeletal Muscle
Mostly absorbed in the small intestine - Muscle weakness and cramps
Aldosterone is the principal hormone regulator in - Paralysis
secretion Gastrointestinal Motility
- Constipation
FUNCTIONS OF POTASSIUM - Ileus
muscular contraction (particularly cardiac) Bladder Function
neuromuscular contraction, including smooth - Urinary Retention
muscles
dietary sources: Asthmatics on salbutamol/albuterol are sometimes
constipated because their medications drive
potassium back into the cell.
 S-T segment depression
POTASSIUM REPLACEMENT Widening of the QRS complex
Maintenance Requirement Progress to ventricular fibrillation
- 20 -30 mEq of KCl per liter of IVF once patient Asystole may also occur
has voidedHypokalemia
- Hypokalemia (ileus, muscle weakness, ECG Request for long lead II.
changes)
o dose of intravenous potassium 0.5-1 mEq/kg,
usually given over 1 hr
o 40 mEq of KCl per liter of IVF once patient
has voided
o maintain a constant conc. of K+ for 3-4 days

Patient should be in an intensive care setting

Fig 11.a ECG changes in hyperkalemia.
attached to a cardiac monitor.
Do not give more than 40 mEq (although doc
sometimes gives 50 mEq); infusion is very painful.
Oral potassium is available (contains 10 mEq) but
does not taste good.

HYPERKALEMIA
Serum K+ level > 6.5 mEq
Present in severe acidosis, renal insufficiency Fig 11.b ECG changes in hyperkalemia.

CAUSES OF HYPERKALEMIA: TREATMENT FOR HYPERKALEMIA

Spurious laboratory value Calcium gluconate stabilizes the heart
Increased intake NaHCO3 stabilizes the heart in 30 min
Transcellular shifts: Glucose and insulin increased glucose (and
- Acidemia consequently K+) uptake into cells
- Rhabdomyolysis Nebulized salbutamol very fast uptake of K+ into
- Tumor lysis syndrome skeletal muscles (to be used as initial treatment only)
- Hemolysis Loop diuretic removes K+ through urinary excretion
- Digitalis toxicity Kayexalate
- Beta blockers Hemodialysis or peritoneal dialysis
- Exercise 2 goals: stabilize the heart to prevent arrhythmia,
- Insulin deficiency and to remove potassium in the body. Remember:
Decreased excretion: medicines used to stabilize the heart do not help in
- Renal failure removing potassium from the body.
- Primary adrenal disease
- Renal tubular disease
- Drugs
o ACE inhibitors CALCIUM
o K+ sparing diuretics 99% found in the bones
o Cyclosporin IMPORTANCE: blood coagulation, cellular
o NSAIDs communication, exo/endocytosis, muscle
o Trimethoprim contraction, neuromuscular transmission
Adequate intake to permit skeletal growth and
ECG CHANGES IN HYPERKALEMIA mineralization
Wide, tall and tented (peaked) T waves Tight regulation of serum Ca++ concentration to
permit normal physiologic function
Prolonged P-R interval
Wide, flat or absent P wave CAUSES OF HYPOCALCEMIA:
 Early neonatal hypocalcemia infants at risk include
infants of diabetic mothers, preterm infants and ACID-BASE BALANCE MECHANISMS
infants with perinatal asphyxia controlled by buffers, lungs, kidneys
Late neonatal hypocalcemia
Late neonatal hypocalcemia occurs if neonates are BUFFER SYSTEMS
fed cows milk with high phosphate content. Buffer is a substance that reduces the change in free
Maternal hypercalcemia hydrogen ion concentration of a solution through the
Hypoparathyroidism addition of an acid or base
Vitamin D deficiency - Bicarbonate buffer system
Inadequate intake - Non bicarbonate buffer system
o protein histidine
TREATMENT o organic phosphates
HYPOCALCEMIA: o bone
- 1-2 ml/kg of 10% Calcium gluconate
Cardiac monitoring is done if calcium gluconate is PULMONARY MECHANISM
given every 8 hours; not done if given IV. Modifies pH by changing PCO2 levels
Ex. RR excretion of CO2 PCO2 pH
HYPERCALCEMIA
- Hydration with normal saline (aggressive) RENAL MECHANISM
- Glucocorticoids Reabsorption of nearly all the filtered bicarbonate
- Calcitonin Excretion of hydrogen ion and addition of new
bicarbonate to the blood
MAGNESIUM
3rd most common intracellular cation ASSESSMENT OF ACID BASE DISORDERS
50-60% is found in the bones PCO2
Necessary cofactor for a lot of coenzymes [H+] = 24 + HCO3
Normal plasma value
- 1.5 2.3 mg/dl Acidemia pH below 7.35
- 1.2 1.9 mEq/L Acidosis: an increase in hydrogen ion concentration
- 0.62 0.94 mmol/L Alkalemia pH above 7.45
Treatment for hypomagnesemia (IM/IV) Alkalosis: a decrease in hydrogen ion concentration
- 25-50 mg/kg of magnesium sulfate
METABOLIC ACIDOSIS
FUNCTIONS OF MAGNESIUM : 3 Basic Mechanisms:
helps maintain intracellular activity 1. Loss of bicarbonate from the body
affects muscle function, especially relaxation 2. Impaired renal ability to excrete acid
helps maintain normal heart rhythm 3. Addition of acid to the body (exo/endo)
promotes vasodilation of peripheral arterioles
Anion Gap = [Na+] [Cl-] + [HCO3-]
Normal value = 8 16

TREATMENT Normal anion gap

HYPOMAGNESEMIA Diarrhea
- 25-50mg/kg of magnesium sulfate (0.05-0.1 Renal tubular acidosis
mL/kg of a 50% solution)
Increased anion gap
ACID-BASE BALANCE Lactic acidosis (ex. due to septicemia)
Ketoacidosis (ex. due to diabetes)
Normal pH = 7.35 7.45 Liver failure
Acid donates a hydrogen ion
Base accepts a hydrogen ion
 Test arterial blood gas (ABG) when checking for anion
gap.

CLINICAL MANIFESTATIONS:
Deep sighing breathing (Kussmaul breathing)
Pinkish cheeks/lips
Hepatomegaly

TREATMENT: Sodium bicarbonate

mEq required = desired HCO3 actual HCO3 x k (see
below) x wt in kg
k = 0.5 0.6

EMPIRICAL TREATMENT
2 mEq/kg slow infusion not to exceed 3 doses
Precautions:
- Needle should be securely in vein
- Give slowly
- Excessive administration should be avoided to
prevent post acidotic tetany and hypernatremia

Be strong and take heart, all you who hope in the Lord.
Psalm 31:24

References:
Dr. Mendozas Lecture and Slides,
SERVIAM, JAX notes
Internet (pictures, articles)

Prepared by: Ena, Nadine, Andy

Edited by: Andy

Sources:
Dr.
Dr. Rufon's
Rufon's ppt
ppt
Andrew's Dermatology
JAX
JAX notes
notes
Google: pictures
Proofreader:
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