1

FLUIDS

60 %

Intracellular Fluid 40% or 2/3 Extracellular Fluid 20% or 1/3

Arterial Fluid
2%
Intravascular Interstitial
5% or 1/4 15% or 3/4

Venous
Fluid 3% Transcellular fluid 1-2%
ie csf, pericardial, synovial,
pleural,lymph system,
intraocular

FLUIDS - approximately 3L of the average

6L of blood is
•Maintain homeostasis made up of plasma
•Ensure adequate tissue perfusion
•Help maintain body temperature and cell Interstitial space - contains fluids that
shape surround the cell; about 11-12 liters
•Help transport nutrients, gases and wastes
Transcellular space - contains 1 L of fluid
ex. Cerebrospinal, pericardial,
Fluids synovial, intraocular and digestive secretion
•60% of an adult’s body weight Sources of Fluids
* 70 Kg adult male: 60% X 70= 42 Fluid Intake
Liters 1. Exogenous sources
•Infants = more water •Fluid intake
•Elderly = less water oral liquids – 1, 300 ml
•More fat = ↓water water in food – 1, 000 ml
water produced by metabolism – 300 ml
•More muscle = ↑water
•Infants and elderly - prone to fluid •IVF
imbalance •Medications
•Blood products
Factors that influence amount of body
fluids: 2. Endogenous sources
•By products of metabolism
1. age
•secretions
- younger people have higher
percentage of body fluid than older people
Fluid Output
Sensible loss
2. gender
- male > women •Urine - 1, 500 ml
•Fecal losses – 200 ml
3. body fats
- obese people have less fluids than
Insensible loss
thin people
(fat cells contain little water) •skin – 600 ml
•Lungs – 300 ml
Intravascular space - fluid within the blood
vessels , contains plasma

Third-space fluid shift/
Third “spacing”
- loss of ECF into a space that does
not contribute to equilibrium between ICF
and ECF
- ie ascites, burns, peritonitis, bowel
obstruction, massive bleeding
Mechanisms of Body Fluid Movement (i.e.
movement of solutes, solvents across
different extracellular locations)
A. Osmosis: water is mover; water
moves from lower concentration to higher
concentration
1. Normal Osmolality of ICF and ECF:
275 – 295 mOsm/kg
Types of solutions according to osmolality
a. Isotonic: all solutions with
osmolality same as that of plasma
Body cells placed in isotonic fluid:
neither shrink nor swell
b. Hypertonic: fluid with greater
concentration of solutes than plasma
Cells in hypertonic solution: water
in cells moves to outside to equalize
concentrations: cells will shrink
c. Hypotonic: fluid with lower
concentration of solutes than plasma
Cells in hypotonic solution: water
outside cells moves to inside of cells: cells
will swell and eventually burst (hemolyze)
•Different intravenous solutions, used to
correct some abnormal conditions,
categorized according to osmolality:
a. Hypertonic: 5%glucose, 45% NaCl
solution
b. Isotonic: 9% NaCl, Lactated
Ringers solution
c. Hypotonic: 45% NaCl
B. Diffusion: solute molecules move
from higher concentration to lower
concentration
1. Solute, such as electrolytes, is the
mover; not the water
2. Types: simple and facilitated
(movement of large water-soluble
molecules)
C. Filtration: water and solutes move
from area of higher hydrostatic pressure to
lower hydrostatic pressure
1. Hydrostatic pressure is created by
pumping action of heart and gravity against
capillary wall
2
2. Usually occurs across capillary
membranes
D. Active Transport: molecules move
across cell membranes against concentration
gradient; requires energy, e.g. Na – K pump
Transport Mechanisms
•fluids from different compartments move
from one compartment to the other to
maintain fluid balance.
•movement is dictated by the transport
mechanism principle :
A. PASSIVE
B. ACTIVE TRANSPORT
A. Passive Transport Process
– substances transported across the
membrane w/o energy input from the cell
- high to low concentration
2 Types of Passive Transport
1. Diffusion – substances/solutes move from
high concentration to low concentration
ie exchange of O2 and CO2 b/w pulmonary
capillaries and alveoli
2. Filtration – water and solutes forced
through membrane by fluid or hydrostatic
pressure from intravascular to interstitial
area
- solute containing fluid (filtrate)
from higher pressure to lower pressure
- an example of this process is urine
formation
- increased hydrostatic pressure is
one mechanism producing edema
B. Active Transport Process
-Cell moves substances across a membrane
through ATP because:
-They may be too large
-Unable to dissolve in the fat core
-Move uphill against their concentration
gradient
Types of Active Transport
1. Active transport – requires protein carriers
using ATP to energize it
ie Amino acids
Sodium potassium pump – 3Na out, 2K
in
2. Endocytosis – moves substances into the
cell
3. Exocytosis – moves substances out of the
cell
Osmosis
 3

•Movement of water from low solute to high •10% Dextran 40 in 5% Dextrose isotonic
solute concentration in order to maintain (252 mOsm/L)
balance between compartments. •Lactated Ringer’s Solution isotonic
•Osmotic pressure – amount of hydrostatic - Na 130 mEq/L
pressure needed to stop the flow of water by - K 4 mEq/L
osmosis -Ca 3 mEq/L
•Oncotic pressure – osmotic pressure - Cl 109 mEq/L
exerted by proteins - 273 mOsm/L
Rx:hypovolemia, burns, fluids lost as
Types of Fluid bile/diarrhea, acute blood loss
Tonicity CI: ph>7.5, lactic acidosis, renal
failure(cause HyperK)
•This is the concentration of solutes in a
solution
Hypotonic Fluid
•A solution with high solute concentration is - fluid will enter the cell, the cell
considered as HYPERTONIC will swell
•A solution with low solute concentration is Hypotonic Fluids
considered as HYPOTONIC
•0.45% NaCl (half strength saline)
•A solution having the same tonicity as that - provides Na, Cl and free water
of body fluid or plasma is considered - Na 77 mEq/L
ISOTONIC - Cl 77 mEq/L
- 154 mOsm/L
•In a HYPERTONIC solution, fluid will go Rx: hypertonic dehydration, Na and Cl
out from the cell, the cell will shrink. depletion, gastric fluid loss
CI : 3rd space fluid shifts and inc
•In a HYPOTONIC solution, fluid will enter ICP
the cell, the cell will swell.
•In an ISOTONIC solution, there will be no Hypertonic Fluid
movement of fluid. - fluid will go out from the cell, the
cell will shrink
Isotonic Fluid Hypertonic Fluids
- no movement of fluid.
Isotonic Fluids •3% NaCl (hypertonic saline)
•0.9% NaCl/ Normal Saline/NSS - no calories
-Na=154 - Na 513 mEq/L
-Cl=154 - Cl 513 mEq/L
-308 mOsm/L -1026 mOsm/L
- not desirable as routine maintenance Rx: critical situations to treat HypoNa, assist
solution in removing ICF excess
- only solution administered with blood CI: administered slowly and cautiously (IVF
products overload and pulmonary edema)
Rx: hypovolemia, shock, DKA,
metabolic alkalosis, hypercalcemia, mild NA •5% NaCl
deficit •D10W - 10% Dextrose in water hypertonic
CI: caution in renal failure, heart (505 mOsm/L)
failure and edema •D10W - 20% Dextrose in water hypertonic
(1011 mOsm/L)
•D5W - 5% Dextrose in water •D50W - 50% Dextrose in water hypertonic
- 170 cal and free water (1700 mOsm/L)
- 252 mOsm/L •D5NS - 5% Dextrose & 0.9NaCl
Rx: hypernatremia, fluid loss and hypertonic (559 mOsm/L)
dehydration •D10NS - 10% Dextrose & 0.9NaCl
CI: early post op when ADH inc d/t stress, hypertonic (812 mOsm/L)
sole treatment in FVD (dilutes plasma), head •D5LR - 5% Dextrose in Lactated Ringers
injury (inc ICP), fluid resuscitation hypertonic (524 mOsm/L
(hyperglycemia), caution in renal and
cardiac dse (fluid overload), px with NA Colloid solutions
deficiency (peripheral circulatory collapse
and anuria) •Dextran 40 in NS or 5% D5W

- volume/plasma expander
- decrease coagulation
- remains for 6H in circulatory system
Rx: hypovolemia in early shock, improve
microcirculation (dec RBC aggregation)
CI: hemorrhage, thrombocytopenia, renal
disease and severe dehydration
Mechanisms that Regulate Homeostasis:
How the body adapts to fluid and electrolyte
changes
A.Thirst: primary regulator of water intake
(thirst center in brain)
B.Kidneys: regulator of volume and
osmolality by controlling excretion of water
and electrolytes
C.Renin-angiotension-aldosterone
mechanism: response to a drop in blood
pressure; results from vasoconstriction and
sodium regulation by aldosterone
D.Antidiuretic hormone: hormone to
regulate water excretion; responds to
osmolality and blood volume
E.Atrial natriuretic factor: hormone from
atrial heart muscle in response to fluid
excess; causes increased urine output by
blocking aldosterone
Organs involved in homeostasis
•Kidneys
•Lungs
•Heart
•Adrenal glands
•Parathyroid glands
•Pituitary glands
•Other mechanisms
1. baroreceptor
2. renin-angiotensin-aldosterone
system
3. ADH and thirst
4. osmoreceptor
5. release of atrial natriuretic
peptide
•Organs involved in homeostasis
A. Kidney - vital to regulation of fluid and
electrolytes
- filters 170 L of plasma everyday
- urine output in an adult is 1-2
liters / day
- releases RENIN
- regulates sodium and water
balance
Functions include :
1. regulation of ECF volume and
osmolality by selective retention and
excretion of body fluids
2. regulation of electrolytes levels in the
ECF by selective retention of needed
4
substance and excretion of unneeded
substance
3. regulation of pH of the ECF by
retention of hydrogen ions
4. excretion of metabolic waste and toxic
substances
B. Heart and blood vessels - pumping action
of the heart to maintain renal perfusion
C. Lungs - maintain homeostasis through
exhalation
-remove approximately 300 – 400 ml of
water daily
-loss is greater if there is increase in
respiratory depth or rate or in dry climate
D. Pituitary function - hypothalamus
manufactures ADH
- ADH used for water retention or
excretion of water by the kidney and in
regulating blood volume
E. Adrenal function - secretes aldosterone,
has effect on fluid regulation
- secretes also cortisol – has a fraction effect
of aldosterone
F. Parathyroid function - regulates calcium
and phosphate
- influences bone resorption , Ca absorption
from the intestine, and Ca reabsorption from
the renal tubules
•Other mechanisms:
1. baroreceptors - are small nerve receptors
that detect pressure within blood vessels and
transmit information to the CNS
- responsible for monitoring for circulating
volume and they regulate sympathetic and
parasympathetic neural activity and
endocrine function
types: low-pressure
high-pressure
•High pressure - are nerve endings in the
aortic arch and in the cardiac sinus
- another is seen in the afferent arteriole of
the juxtaglomerular apparatus of nephron
•Low pressure - are located in cardiac atria,
particularly in the left atria
2. renin-angiotensin – aldosterone system:
- renin : an enzyme that convert
angiotensinogen to
angiotensin I, it is released from
juxtaglomerular cells of the kidney to
decrease renal perfusion
 5

then angiotensin I is converted to 1. The Kidney

angiotensin II by angiotensin converting •Regulates primarily fluid output by urine
enzymes ,w/c is a vasoconstrictor w/c in
formation 1.5L
turn increases arterial perfusion and
stimulates thirst, •Releases RENIN
•Regulates sodium and water balance
aldosterone is released
2. Endocrine regulation
factors that influence aldosterone secretion:
1. increased release of renin
•thirst mechanism – thirst center in
2. increased serum
hypothalamus
potassium
3. decreased Na serum
4. ACTH increase
•ADH increases water reabsorption on
collecting duct
3. ADH and THIRST - have important role
in maintaining sodium concentration and •Aldosterone increases Sodium and water
oral intakes of fluids retention retention in the distal nephron

thirst: oral intake is controlled by thirst •ANP Promotes Sodium excretion and
center located in the hypothalamus : inhibits thirst mechanism
serum
osmolality 3. Gastro-intestinal regulation
or blood - GIT digests food and absorbs water
volume - Only about 200 ml of water is
excreted in the fecal material per day
stimulate thirst
center 4. Heart and Blood Vessel Functions
- pumping action of heart circulates blood
ADH - controls water excretion through kidneys
- determines concentration of urine
5. Lungs – insensible water loss through
4. osmoreceptors - located in the surface of respiration
hypothalamus Other Mechanisms
- sense changes in Na 1. Baroreceptors – carotid sinus and aortic
concentration arch
- causes vasoconstriction and increased
osmotic pressure (neurons become blood pressure
dehydrated)
Dec arterial pressure SNS inc
releases impulses to cardiac rate, contraction, contractility,
posterior pituitary to circulating blood volume, constriction of
renal arterioles and increased aldosterone
release ADH
2. Osmoreceptors – surface of hypothalamus
increases permeability of membrane to senses changes in Na concentration

H2O (kidney, causing Inc osmotic pressure neurons

reabsorption of water and decreased dehydrated release ADH
urine output)

5. Release of atrial natriuretic peptide - KIDNEY

released by cardiac cells in the atria of the •Nephron: glomerulus and tubule
heart in response to increased atrial •Filtration
pressure •Retention/ Reabsorption
•Excretion
- action of this is direct opposite of RAAS •170-180 L/day
and decreases blood pressure and volume
•Filtrate= urine
(1-2 L urine/ day)
- ANP level is 20 to 77 pg /ml (ng/ml)
•Fluid excess excretes dilute urine (rids
Regulation of Body Fluid body of excess fluid while conserving
electrolytes)
 6

–Urine SG is low
ADH (Antidiuretic hormone) –Hct is high
•Vasopressin RAAS (Renin-Angiotensin-Aldosterone
System)
•Water-retainer •To help maintain a balance of sodium and
•Hypothalamus produces ADH water, a healthy blood volume and blood
•Posterior pituitary gland stores and releases pressure, the juxtaglomerular cells near
ADH each glomerulus secrete RENIN
•Restores blood volume by reducing
•Leads to production of Angiotensin II, a
powerful vasoconstrictor
diuresis and increasing water retention
•Angiotensin II causes peripheral
ADH vasoconstriction, stimulating production of
Low blood volume/ Aldosterone
Pituitary gland •Both increase blood pressure.
Increased serum osmolality
secretes ADH Aldosterone Production
Decreased JG cells
into the bloodstream Renin travels
blood flow to the secrete
ADH causes the Water to the
retention glomerulus Renin
Kidneys to retain water increases liver
blood
volume/ decreases
Renin converts Angiotension 1
serum osmolality Angiotensin 1
ADH Regulation Angiotensin in travels to the
•ADH - produced by the Hypothalamus in the lungs is
the liver to lungs
- stored and secreted by the posterior
converted to
pituitary gland
Angiotensin 1
•less water in plasma,ADH secreted to Angiotensin II
conserve water by reducing urine output
•fluid overload in plasma, ADH secretion
stops to excrete fluid in the kidneys by Angiotensin II Angiotensin II
increasing urine output travels to the stimulates the
ADH Disorder Adrenal glands adrenal glands to
produce
•Abnormally high ADH concentration - Aldosterone
SIADH Aldosterone
reduced urine output (oliguria)
water retention (fluid overload)
Angiotensin II Aldosterone
•Abnormally low ADH – Diabetes Insipidus Sodium and
increased urine output (polyuria) stimulates the causes
water loss (fluid deficit) kidneys water retention
adrenal glands to to
ADH Disorder retain sodium leads to increased
produce Aldosterone and water
•SIADH fluid volume and
–Abnormally high ADH concentration
–urine output is reduced (oliguria)
–water retention (fluid overload) sodium level
–Urine SG is high (normal: 1.005 – 1.030)
–Hct is low (43-48%)
Aldosterone Disorders
•DI •Addison’s Disease
–Abnormally low ADH
–Abnormally low aldosterone
–urine output is increased (polyuria)
–water loss (fluid deficit) –Serum Na is low, serum potassium is high
 7

–FVD decrease ADH

•Cushing’s Disease
–Abnormally high aldosterone
–Serum Na is high, serum potassium is low
–FVE
ANP (Atrial Natriuretic Peptide)
•Cardiac hormone
•Stored in the cells of the atria
•Released when atrial pressure increases
•Counteracts the effects of the RAAS by
decreasing blood pressure and reducing
intravascular blood volume
•When blood volume and BP rise and
stretch the atria, ANP shuts off RAAS
ANP
•Suppresses serum renin levels
•Decreases aldosterone release from the
adrenal glands
•Increases glomerular filtration, which
increases urine excretion of sodium and
water
•Decreases ADH release from the posterior
pituitary gland
•Reduces vascular resistance by causing
vasodilation
Examples of causes of atrial stretching
(which result to increased release of ANP)
•Orthostatic changes
•Atrial tachycardia
•High sodium intake
•Sodium chloride infusions
•Use of drugs that cause vasoconstriction
•Physiology/pathophysiology
increased blood
volume
increased blood
pressure
increased stretch of
atria
increased
ANP release
vascular resistance
increase GFR w/c increases
urinary excretion of Na and
Decrease blood pressure
water
Suppression of serum renin
decrease vascular
volume
decrease BP,
decrease preload and afterload
Thirst mechanism
•Regulated by the hypothalamus
•Stimulated by an increase in ECF and
drying of mucous membrane
•Causes a person to drink fluids, which is
absorbed by the intestines, moved to the
bloodstream and distributed between the
compartments
•Leads to increased amount of fluid in the
body and a decrease in concentration of
solutes
Decreased Blood Volume
THIRST mechanism
•ADH secretion is increased
•ANP secretion is decreased
•RENIN secretion is increased
•BARORECEPTOR vasoconstricton
•ALDOSTERONE secretion is increased
Increased Blood Volume
•NO THIRST mechanism
•ADH secretion is decreased
•ANP secretion is increased
•RENIN secretion is increased
•BARORECEPTOR vasodilation
•ALDOSTERONE decreased
Fluid status can be assessed through:
•Mucus membrane
•Skin integrity
•Body weight
•Jugular vein
•BP, PAWP 6-12 mm Hg
•CVP (most accurate) 0-7 mm Hg or 5-10
cm of H2O
•I&O
•Pulse
•Temperature
 8

•Lung sound and heart sound •byproduct of muscle metabolism &

•Urine output excreted
•Urine SG 1.005-1.030 by kidneys regardless of fluid
•Hematocrit 48% intake, diet, etc.
•Plasma osmolality •measures kidney function; 50% renal
•LOC function lost BEFORE ↑ in serum
creatinine level
Evaluation of fluid status
Osmolality – concentration of fluid that •better indicator of renal function
affects movement of water between fluid • .7 to 1.5 mg/dl
compartments by osmosis
- measures the solute concentration
per kg in blood and urine Hematocrit - indication of hydration status
- measure of solution’s ability to - measures the volume percentage of
create osmotic pressure and affect the red blood
movement of sodium cells in whole blood and normally
ranges from
- reported as mOsm/kg
- normal value= 280-300 mOsm/kg 44% to 52% for male
39% - 47% in females
Osmolarity – concentration of solutions
- measures the solute concentration hematocrit due to: 1. dehydration
per L in blood and urine 2. polycythemia
- mOsm/L
hematocrit due to: 1. overhydration
2. anemia
urine specific gravity - measures the kidneys
ability to excrete or conserve water

urine specific gravity: 1.010 - 1.025 •Urine sodium values: change with sodium
intake and status of fluid volume
Blood urea nitrogen - made up of urea, end
product of metabolism of protein - normal level ranges from 50 -
220mEq/24h
10-20mg/dl (3.5-7mmol/l) - used to assess volume status and
in the diagnosis of hyponatremia and acute
BUN: not most reliable indicator of renal renal failure
disease BUN:creatinine ratio better indicator
Normal 10:1. Fluid volume disturbances
•I and O must be equal
increased BUN due to:
•2.5 L per day
1. renal function •Fluid volume deficit (hypovolemia)
2. GI bleeding
3. dehydration
•Fluid volume excess (hypervolemia)
4. increased protein
intake
I&O Imbalance
5. fever and sepsis
Fluid Volume Deficit
decreased BUN due to : •↑output, normal intake
1. end-stage liver •Normal output, ↓ intake
disease •No intake
2. low protein
intake
3. starvation Fluid Volume Excess
4.condition that
expands fluid volume •↑ intake, normal output
ex. •Normal intake, ↓ output
pregnancy •No output

Creatinine
 9

1. Fluid volume deficit •Isotonic fluids ie LR lactated ringers or

- occurs when loss of ECF volume
exceeds the intake of fluid
causes:
1. abnormal fluid losses
vomiting, diarrhea, GI
suctioning and sweating
Diabetes Insipidus
Adrenal insufficiency
Osmotic diuresis
Hemorrhage
3rd space fluid shift
2. decreased intake
.9% NaCl for hypotensive patients to expand
plasma volume
Nursing Management
•measure I and O accurately
•monitoring of body weight
- loss of .5 kg means a loss of 500ml
•monitoring of V/S
•skin turgor assessment
•Assess CVP, LOC, breath sounds and skin
color
•Monitor urinary concentration
•Monitor mental function

signs and symptoms :

1. acute weight loss 2. fluid volume excess
2. decreased skin turgor (hypervolemia)
3. oliguria - refers to an isotonic expansion of
4. concentrated urine the ECF caused by the abnormal retention
5. postural hypotension, of water and Na in approx. same proportion
weak and rapid heart rate - usually 2nd to increase in total
6. flattened neck veins, body Na content
decreased CVP, cool clammy skin
7. Thirst, anorexia Pathophysiology:
8. Muscle weakness and 1. related to simple fluid
cramps overload
2. diminished function of
the homeostatic
Assessment of FVD mechanism responsible for
•ICF regulating fluid balance
cellular dehydration
Causes of FVE
•ITF
skin poor skin turgor •Heart failure
•IVF •renal failure
artery ↓BP, pulse (rapid thready) •cirrhosis of the liver
vein ↓CVP
•consumption of excessive amount of salt
assessment : •Excessive administration of Na containing
1. elevated BUN fluids in a patient w/ impaired regulatory
2. elevated Hct. mechanism
3. serum electrolyte changes
may also exist
•SIADH
1. hypokalemia- GI
and renal losses Clinical Manifestations
2. hyperkalemia- •Distended neck veins
adrenal insufficiency •Tachycardia
3. hyponatremia- •Inc weight
increased thirst and ADH release
4. hypernatremia- •Increased urine output
increased insensible losses and •Shortness of breath and wheezing/ crackles
diabetes •Inc CVP
insipidus
Medical Management
•Edema
•increased BP
•Oral intake when mild
•increased pulse pressure
•IV route, acute or severe

Assessment of FVE
•ICF
cellular edema - ↓LOC
pulmonary edema - crackles (bibasilar),
wheezing,
shortness of breath, Inc RR
•ITF
skin - bipedal pitting edema, periorbital
edema and ANASARCA
•IVF
artery - ↑BP, pulse (rapid bounding)
vein - ↑CVP
Edema
•common manifestation of FVE
•d/t inc capillary fluid pressure, decreased
capillary oncotic pressure, increased
interstitial oncotic pressure
•Localized or generalized
•Etiology: obstruction to lymph flow,
plasma albumin level < 1.5-2 g/dl, burns and
infection, Na retention in ECF, drugs
•Labs: Dec Hct, respiratory alkalosis and
hypoxemia, dec serum Na and osmolality,
inc BUN Crea, Dec Urine SG, dec urine Na
level
•Mgmt: diuretics, fluid restriction, elevation
of extremities, elastic compression
stockings, paracentesis, dialysis
Laboratory (FVE)
•Dec BUN
•Dec Hct
•CRF – serum osmolality and Na level dec
•chest x-ray may reveal pulmonary
congestion
Medical Management
•Discontinue administration of Na solution
•Diuretics
ie Thiazide – block Na reabsorption
in
distal tubule
Loop diuretics – block Na reabsorption
in ascending loop of Henle
•Restrict fluid and salt intake
•Dialysis
Nursing Management
•Measure intake and output
•Weigh patient daily
2 lb wt gain = 1 L fluid
10
•Assess breath sounds
•Monitor degree of edema
ie ambulatory – feet and ankles
bedridden – sacral area
•Promote rest – favors diuresis/inc venous
return
•Administer appropriate medication
Electrolytes
•elements or compounds when dissolved in
water will dissociate into ions and are able
to conduct an electric current.
FUNCTIONS:
1. Regulate fluid balance and osmolality
2. Transmission of nerve impulse
3. Stimulation of muscle activity
•ANIONS - negatively charged ions:
Bicarbonate, chloride, PO4-, CHON
•CATIONS - positively charged ions:
Sodium, Potassium, magnesium, calcium
Cations
Sodium , Potassium , Calcium , Magnesium
, hydrogen ions
Anions
Chloride, bicarbonate , phosphate, sulfate,
proteinate ions
•Sodium - positively charged ions , major
cation in the ECF
-important in regulating the volume
of body fluids
-retention of Na- associated with
fluid retention
-loss of Na- decreased volume of
body fluids
•Potassium - major cation in the ICF
•Chloride - major anion in the ECF
•Phosphate - major anion in the ICF
Regulation of Electrolyte Balance
1. Renal regulation
•Occurs by the process of glomerular
filtration, tubular reabsorption and tubular
secretion
•Urine formation

–If there is little water in the body, it is
conserved
–If there is water excess, it will be
eliminated
2. Endocrinal regulation
•Aldosterone promotes Sodium retention
and Potassium excretion
•ANP promotes Sodium excretion
•Parathormone increased bone resorption
of Ca, inc Ca reabsorption from renal tubule
or GI tract
•Calcitoninoppose PTH
•Insulin and Epinephrine – promotes uptake
of Potassium by cells
The Cations
•SODIUM
•POTASSIUM
•CALCIUM
•MAGNESIUM
SODIUM (Na)
•MOST ABUNDANT cation in the ECF
•135-145 mEq/L
•Aldosterone increases sodium
reabsorption
•ANP increases sodium excretion
•Cl accompanies Na
FUNCTIONS:
1. assists in nerve transmission and muscle
contraction
2. Major determinant of ECF osmolality
3. Primary regulator of ECF volume
a. HYPERNATREMIA
•Na > 145 mEq/L
•Assoc w/ water loss or sodium gain
•Etiology: inadequate water intake,
excessive salt ingestion /hypertonic feedings
w/o water supplements, near drowning in
sea water, diuretics, Diabetes mellitus/
Diabetes Insipidus
S/SX: polyuria, anorexia, nausea, vomiting,
thirst, dry and swollen tongue, fever, dry and
flushed skin, restlessness, agitation,
seizures, coma, muscle weakness, crackles,
dyspnea, cardiac manifestations dependent
on type of hypernatremia
11
Dx: inc serum sodium and Cl level, inc
serum osmolality, inc urine sp.gravity, inc
urine osmolality
Mgmt: sodium restriction, water restriction,
diuretics, isotonic non saline soln. (D5W) or
hypotonic soln, Desmopressin Acetate for
Diabetes Insipidus
Nsg considerations
History – diet, medication
Monitor VS, LOC, I and O, weight, lung
sounds
Monitor Na levels
Oral care
initiate gastric feedings slowly
Seizure precaution
b. HYPONATREMIA
•Na < 135 mEq/L
•Etiology: diuretics, excessive sweating,
vomiting, diarrhea, SIADH, aldosterone
deficiency, cardiac, renal, liver disease
•Dx: dec serum and urine sodium and
osmolality, dec Cl
•s/sx: headache, apprehension, restlessness,
altered LOC, seizures(<115meq/l),coma,
poor skin turgor, dry mucosa, orthostatic
hypotension, crackles, nausea, vomiting,
abdominal cramping
Mgmt: sodium replacement, water
restriction, isotonic soln for moderate
hyponatremia, hypertonic saline soln for
neurologic manifestations, diuretic for
SIADH
Nsg. Consideration
Monitor I and O, LOC, VS, serum
Na
Seizure precaution
diet
Potassium (K)
•MOST ABUNDANT cation in the ICF
•3.5-5.5 mEq/L
•Major electrolyte maintaining ICF balance
•maintains ICF Osmolality
•Aldosterone promotes renal excretion of
K+
•Mg accompanies K
FUNCTIONS:
 12

1. nerve conduction and muscle contraction ECG - flattened , depressed T waves,

2. metabolism of carbohydrates, fats and presence of “U” waves
proteins ABGs - metabolic alkalosis
3. Fosters acid-base balance
Medical Mgmt:
a. HYPERKALEMIA diet ( fruits, fruit juices, vegetables, fish,
whole grains, nuts, milk, meats)
•K+ > 5.0 mEq/L oral or IV replacement

•Etiology: IVF with K+, acidosis, hyper- Nsg mgmt:

alimentation and excess K+ replacement,
decreased renal excretion, diuretics, Cancer
•s/sx: nerve and muscle irritability,
tachycardia, colic, diarrhea, ECG changes,
ventricular dysrythmia and cardiac arrest,
skeletal muscle weakness, paralysis
monitor cardiac function, pulses, renal
function
monitor serum potassium concentration
IV K diluted in saline
monitor IV sites for phlebitis
Normal ECG

•Dx: inc serum K level

Hypokalemia
ECG: peaked T waves and wide QRS
ABGs – metabolic acidosis
Hyperkalemia

Mgmt:
Regulation:
K restriction (coffee, cocoa, tea, dried fruits,
beans, whole grain breads, milk, eggs) •GIT absorbs Ca+ in the intestine with the
diuretics help of Vitamin D
Polystyrene Sulfonate (Kayexalate) •Kidney Ca+ is filtered in the glomerulus
IV insulin and reabsorbed in the tubules
Beta 2 agonist •PTH increases Ca+ by bone resorption,
IV Calcium gluconate – WOF Hypotension inc intestinal and renal Ca+ reabsorption and
IV NaHCo3 – alkalinize plasma activation of Vitamin D
Dialysis
•Calcitonin reduces bone resorption,
Nsg consideration: increase Ca and Phosphorus deposition in
Monitor VS, urine output, lung bones and secretion in urine
sounds, Crea, BUN a. HYPERCALCEMIA
monitor K levels and ECG
observe for muscle weakness and •Serum calcium > 10.5 mg/dL
dysrythmia, paresthesia and GI symptoms
•Etiology: Overuse of calcium supplements
b. HYPOKALEMIA and antacids, excessive Vitamin A and D,
malignancy, hyperparathyroidism, prolonged
•K+ < 3.5 mEq/L immobilization, thiazide diuretic

•Etiology: use of diuretic, corticosteroids •s/sx: anorexia, nausea, vomiting, polyuria,

and penicillin, vomiting and diarrhea, muscle weakness, fatigue, lethargy
ileostomy, villous adenoma, alkalosis,
hyperinsulinism, hyperaldosteronism •Dx: inc serum Ca
ECG: Shortened QT interval, ST segments
•s/sx: anorexia, nausea, vomiting, decreased inc PTH levels
bowel motility, fatigue, muscle weakness, xrays - osteoporosis
leg cramps, paresthesias, shallow
respiration, shortness of breath,
dysrhythmias and increased sensitivity to •Mgmt:
digitalis, hypotension, weak pulse, dilute 0.9% NaCl
urine, glucose intolerance IV Phosphate
Diuretics – Furosemide
IM Calcitonin
Dx: dec serum K level corticosteroids

dietary restriction (cheese, ice cream, milk,
yogurt, oatmeal, tofu)
Nsg Mgmt:
Assess VS, apical pulses and ECG, bowel
sounds, renal function, hydration status
safety precautions in unconscious
patients
inc mobility
inc fluid intake
monitor cardiac rate and rhythm
b. HYPOCALCEMIA
•Calcium < 8.5 mg/dL
•Etiology: removal of parathyroid gland
during thyroid surgery, Vit. D and Mg
deficiency, Furosemide, infusion of citrated
blood, inflammation of pancreas, renal
failure, thyroid CA, low albumin, alkalosis,
alcohol abuse, osteoporosis (total body Ca
deficit)
• s/sx: Tetany, (+) Chovstek’s (+)
Trousseaus’s, seizures, depression, impaired
memory, confusion, delirium, hallucinations,
hypotension, dysrythmia
•Dx:
dec Ca level
ECG: prolonged QT interval
•Mgmt:
Calcium salts
Vit D
diet (milk, cheese, yogurt, green
leafy vegetables)
•Nsg mgmt
monitor cardiac status, bleeding
monitor IV sites for phlebitis
seizure precautions
reduce smoking
Magnesium Mg
•Second to K+ in the ICF
•Normal range is 1.3-2.1 mEq/L
FUNCTIONS
1. intracellular production and utilization of
ATP
2. protein and DNA synthesis
3. neuromuscular irritability
4, produce vasodilation of peripheral arteries
a. HYPERMAGNESEMIA
•M > 2.1 mEq/L
•Etiology: use of Mg antacids, K sparing
diuretics, Renal failure, Mg medications,
13
DKA, adrenocortical insufficiency
•s/sx: hypotension, nausea, vomiting,
flushing, lethargy, difficulty speaking,
drowsiness, dec LOC, coma, muscle
weakness, paralysis, depressed tendon
reflexes, oliguria, ↓RR
•Mgmt: discontinue Mg supplements
Loop diuretics
IV Ca gluconate
Hemodialysis
Nsg mgmt:
monitor VS
observe DTR’s and changes in LOC
seizure precautions
b. HYPOMAGNESEMIA
•Mg < 1.5 mEq/l
•Etiology: alcohol w/drawal, tube feedings,
diarrhea, fistula, GIT suctioning, drugs ie
antacid, aminoglycosides, insulin therapy,
sepsis, burns, hypothermia
•s/sx: hyperexcitability w/ muscle weakness,
tremors, tetany, seizures, stridor, Chvostek
and Trousseau’s signs, ECG changes, mood
changes
•Dx: serum Mg level
ECG – prolonged PR and QT interval, ST
depression, Widened QRS, flat T waves
low albumin level
•Mgmt:
diet (green leafy vegetables, nuts, legumes,
whole grains, seafood, peanut butter,
chocolate)
IV Mg Sulfate via infusion pump
•Nsg Mgmt:
seizure precautions
Test ability to swallow, DTR’s
Monitor I and O, VS during Mg
administration
The Anions
•CHLORIDE
•PHOSPHATES
•BICARBONATES
Chloride (Cl)
•The MAJOR Anion in the ECF
•Normal range is 95-108 mEq/L

•Inc Na reabsorption causes increased Cl
reabsorption
FUNCTIONS
1. major component of gastric juice aside
from H+
2. together with Na+, regulates plasma
osmolality
3. participates in the chloride shift – inverse
relationship with Bicarbonate
4. acts as chemical buffer
a. HYPERCHLOREMIA
•Serum Cl > 108 mEq/L
•Etiology: sodium excess, loss of
bicarbonate ions
•s/sx: tachypnea, weakness, lethargy, deep
rapid respirations, diminished cognitive
ability and hypertension, dysrhytmia, coma
•Dx: inc serum Cl
dec serum bicarbonate
Mgmt:
Lactated Ringers soln
IV Na Bicarbonate
Diuretics
Nsg mgmt:
monitor VS, ABGs, I and O, neurologic,
cardiac and respiratory changes
b. HYPOCHLOREMIA
•Cl < 96 mEq/l
•Etiology: Cl deficient formula, salt
restricted diets, severe vomiting and diarrhea
•s/sx: hyperexcitability of muscles, tetany,
hyperactive DTR’s, weakness, twitching,
muscle cramps, dysrhytmias, seizures, coma
•Dx: dec serum Cl level
ABG’s – metabolic alkalosis
Mgmt:
Normal saline/half strength saline
diet ( tomato juice, salty broth, canned
vegetables, processed meats and fruits
avoid free/bottled water)
Nsg mgmt:
monitor I and O, ABG’s, VS, LOC,
muscle strength and movement
Phosphates (PO4)
•The MAJOR Anion in the ICF
•Normal range is 2.5-4.5 mg/L
•Reciprocal relationship w/ Ca
14
•PTH inc bone resorption, inc PO4
absorption from GIT, inhibit PO4 excretion
from kidney
•Calcitonin increases renal excretion of
PO4
FUNCTIONS
1. component of bones
2. needed to generate ATP
3. components of DNA and RNA
a. HYPERPHOSPHATEMIA
•Serum PO4 > 4.5 mg/dL
•Etiology: excess vit D, renal failure, tissue
trauma, chemotherapy, PO4 containing
medications, hypoparathyroidism
•s/sx: tetany, tachycardia, palpitations,
anorexia, vomiting, muscle weakness,
hyperreflexia, tachycardia, soft tissue
calcification
•Dx: inc serum phosphorus level
dec Ca level
xray – skeletal changes
Mgmt:
diet – limit milk, ice cream, cheese,
meat, fish, carbonated beverages, nuts, dried
food, sardines
Dialysis
Nsg mgmt:
dietary restrictions
monitor signs of impending
hypocalcemia and changes in urine output
b. HYPOPHOSPHATEMIA
•Serum PO4 < 2.5 mg/dl
•Etiology: administration of calories in
severe CHON-Calorie malnutrition
(iatrogenic), chronic alcoholism, prolonged
hyperventilation, poor dietary intake, DKA,
thermal burns, respiratory alkalosis, antacids
w/c bind with PO4, Vit D deficiency
•s/sx: irritability, fatigue, apprehension,
weakness, hyperglycemia, numbness,
paresthesias, confusion, seizure, coma
•Dx: dec serum PO4 level
Mgmt:
oral or IV Phosphorus correction
diet (milk, organ meat, nuts, fish,
poultry, whole grains)
 15

Nsg mgmt: - kidney excrete H and

introduce TPN solution gradually reabsorbs/generates Bicarbonate
prevent infection 2. RESPIRATORY/METABOLIC
ALKALOSIS
- kidney retains H ion and excrete
•Fluids D1 Bicarbonate

•Electrolytes D2 Lung
•Acid-Base D3 -Control CO2 and Carbonic acid content of
ECF
•Burns D3
•Shock D4 1. METABOLIC ACIDOSIS
•GUT D5 - increased RR to eliminate CO2

•MASTERY D6 2. METABOLIC ALKALOSIS

- decreased RR to retain CO2

Acid Base Balance

•Acid •pH - measures degree of acidity and
- substance that can donate or release alkalinity
hydrogen ions - indicator of H ion concentration
ie Carbonic acid, Hydrochloric acid - Normal ph 7.35-7.45

** Carbon dioxide – combines with water to

form carbonic acid •ACIDOSIS
- decreased pH; < 7.35
- increased Hydrogen
•Base
- substance that can accept hydrogen ions
Ie Bicarbonate
•ALKALOSIS
- increased pH-; > 7.45
•BUFFER- substance that can - decreased Hydrogen
accept or donate hydrogen
- prevent excessive changes in pH ACUTE AND CHRONIC
METABOLIC ACIDOSIS
TYPES OF BUFFER -Low pH
1. Bicarbonate (HCO3): carbonic acid buffer
(H2CO3) -Increased H ion concentration
2. Phosphate buffer -Low plasma Bicarbonate
3. Hemoglobin buffer Etiology: diarrhea, fistulas, diuretics, renal
insufficiency, TPN w/o Bicarbonate,
Dynamics of Acid Base Balance ketoacidosis, lactic acidosis
•Acids and bases are constantly produced in S/sx: headache, confusion, drowsiness, inc
the body RR, dec BP, cold clammy skin, dysrrythmia,
•They must be constantly regulated shock
•CO2 and HCO3 are crucial in the balance
•A HCO3:H2CO3 ratio of 20:1 should be
maintained •Dx: ABG – low Bicarbonate, low pH,
Hyperkalemia, ECG changes
•Respiratory and renal system are active in
regulation
•Rx: Bicarbonate for pH < 7.1 and
Bicarbonate level < 10
Kidney monitor serum K
- Regulate bicarbonate level in ECF dialysis
ACUTE AND CHRONIC
1. RESPIRATORY/METABOLIC METABOLIC ALKALOSIS
ACIDOSIS •High pH
•Decreased H ion concentration
 16

•High plasma Bicarbonate ARTERIAL BLOOD GAS ANALYSIS

Etiology: vomiting, diuretic, Evaluating ABG’s

hyperaldosteronism, hypokalemia, excesive Note the pH
alkali ingestion pH = 7.35 – 7.45 (normal)
pH = < 7.35 (acidosis)
s/sx: tingling of toes, dizziness, dec RR, inc pH = > 7.45 (alkalosis)
PR, ventricular disturbances
compensated – normal pH
•Dx:ABG – pH > 7.45, serum Bicarbonate > uncompensated – abnormal pH
26 mEq/L, inc PaCO2

2. Determine primary cause of disturbance

2.1 pH > 7.45
•Rx: restore normal fluid balance a. PaCo2 < 40 mmHg – respiratory
correct hypokalemia alkalosis
Carbonic anhydrase inhibitors b. HCO3 > 26 mEq/L – metabolic alkalosis
ACUTE AND CHRONIC
RESPIRATORY ACIDOSIS 2.2 pH < 7.35
•Ph < 7.35 a. PaCo2 > 40 mmHg – respiratory acidosis
PaCO2 > 42 mmHg b. HCO3 < 26 mEq/L – metabolic acidosis

Etiology: pulmonary edema, aspiration, 3. Determine compensation by looking at

atelectasis, pneumothorax, overdose of the value other than the primary disturbance
seatives, sleep apnea syndrome, pneeumonia

s/sx: sudden hypercapnia produces inc PR,

RR, inc BP, mental cloudinesss, feeling of 4. Mixed acid-base disorders
fullness in head, papiledema and dilated
conjunctival blood vessels

•Dx: ABG – pH < 7.35

PaCO2 - > 42 mmHg
Thank You!
•Rx: improve ventilation
pulmonary hygiene
mechanical ventilation

ACUTE AND CHRONIC

RESPIRATORY ALKALOSIS
•pH > 7.45
•PaCO2 < 38 mmHg
Etiology: extreme anxiety, hypoxemia

s/sx: lightheadednes, inability to

concentrate, numbness, tingling, loss of
consciousness

•Dx: ABG – pH > 7.45

PaCO2 < 35
dec K
dec Ca

Rx: breathe slowly

sedative