Fluid/Electrolytes & Acid

Base Balance
Michael Jenifer RN, MSN
Pathophysiology

Overview

Body cells live in a fluid environment with

electrolytes & fluids maintained within a
narrow range
Electrolyte changes are common but they
affect

Nerve cell function

Muscle cell function
Fluid shifts
Cellular function & blood volume
Can be life threatening

Body Fluid Compartments

Total Body Water (TBW) is 60%

Intracellular Fluid (ICF)

Cellular fluid
2/3 of TBW

Extracellular Fluid (ECF)

Interstitial fluid
Between cells & outside vessels

Intravascular fluid plasma/blood

Other ECF compartments
1/3 of TBW

Fat is hydrophobic

Distribution of Body Fluids (contd)

Pediatrics
75% to 80% of body weight
Susceptible to significant changes in
body fluids

Dehydration in newborns

Aging
Decreased percent of total body water

Increase adipose and decrease muscle

mass
Renal decline
Diminished thirst perception

Body Fluids

Water sources
Drinking, food water & by product of oxidative
metabolism

Water excretion
Renal, stool & vaporization of skin & lungs

Infants
High water weight & immature kidneys

Elderly
Decreased fat masses, decreased muscle mass
& decreased renal efficiency
Diminished thirst perception

Water Movement

Osmosis
Movement of water through a semi permeable
membrane from a region of higher
concentration to one of lower concentration

Na ECF determines water balance

K ICF
Active transport
ICF proteins & non-diffusible substances

Water Movement

Hydrostatic (blood) pressure forces water

out
Oncotic pressures pull water in
Plasma oncotic pressure is usually
constant because proteins normally dont
cross vessels
Starling hypothesis
Net filtration = forces favoring filtration minus
forces opposing filtration

Capillary membrane integrity is important

Fluid Movement Between Plasma and

Interstitial Space

Net Filtration

Forces favoring filtration:

Capillary hydrostatic pressure
(blood pressure)
Interstitial oncotic pressure (waterpulling)

Forces favoring reabsorption:

Plasma oncotic pressure (waterpulling)
Interstitial hydrostatic pressure

Edema

Fluid accumulation in interstitial

areas
Why?
Increased capillary hydrostatic pressure
Lowered plasma oncotic pressure
Increased membrane permeability
Lymphatic obstruction

Why Do We Get Edema

Fluid Movement Formula

Q= (BHP + IFOP) _ (IFHP + BOP)
(from vessel)
(to vessel)
Q = fluid movement
BHP = blood hydrostatic pressure
IFOP = interstitial fluid osmotic pressure
IFHP = interstitial fluid hydrostatic pressure
BOP = blood osmotic pressure

Causes of Hydrostatic Pressure

Increase

Thrombophlebitis
Hepatic obstruction
Tight clothing
Prolonged standing
Heart & renal failure

Causes of Lowered Plasma

Oncotic Pressures

Plasma albumin production decrease

Liver disease
Protein malnutrition

Plasma protein loss

Glomerular kidney disease
Serous wound drainage
Burns
Liver cirrhosis

Causes of Increased Membrane

Permeability

Inflammatory & immune responses

Trauma & burns

Neoplastic disease
Allergic reactions

Causes of Lymphatic Obstructions

Surgical removal
Inflammation
Tumors

Clinical Manifestations of Edema

Localized
Usually limited to site of trauma
Organ edema

Cerebral & pulmonary

Effusions
Pulmonary, cardiac, ascities

Generalized
More uniform distribution in interstitial
space
Dependent edema

Clinical Manifestations of Edema

Weight gain, Swelling, Puffiness

Increases distance of nutrient/waste
movement
Impairs blood flow
Entrapment in the 3rd space

Sodium and Chloride Balance

Sodium
Primary ECF cation
Regulates osmotic forces, thus water
Roles

Neuromuscular irritability, acid-base

balance, and cellular chemical reactions and
membrane transport

Chloride
Primary ECF anion
Provides electroneutrality

Sodium & Chloride Balance

Sodium
90% of ECF cations
Partners with anions chloride & bicarbonate to
control osmotic forces
Works with potassium & calcium to maintain
irritability & acid base balance

Chloride
Major anion in ECF
Inverse concentration relationship with HCO3

Sodium & Chloride Balance

Kidneys control Na concentration

Hormonal mediators
Aldosterone

Secreted by the adrenal cortex

Increases reabsorption of Na & K secretion

Natriuretic hormones

Promote excretion of Na

Water Balance

Kidneys & hormones maintain water

& sodium levels
Regulated by ADH & thirst
2% BW loss or increase in serum
osmolality signals thirst via
osmoreceptors
ADH increases permeability of renal
tubules to water

Sodium and Chloride Balance (contd)

Renin-angiotensin-aldosterone
system
Aldosteroneleads to sodium and
water reabsorption back into the
circulation and potassium and
hydrogen secretion to be lost in
urine

Natriuretic peptides

Renin-Angiotensin-Aldosterone System

Water Balance System

Electrolyte Distribution
ECF
142
5
5
2
154
24
104
2
16
8
154

Cations

ICF
10
156
4
26
196

Na
K
Ca
Mg
Totals
Anions
Bicarb
12
Chloride
4
Phosphate 100
Proteins
54
Others
6
Totals
176

Isotonic Fluid Imbalances

TBW changes proportional to

electrolytes
Isotonic fluid loss

ECF or plasma loss

Hemorrhage, wound drainage sweating
Weight loss, skin dryness, decreased u/o

Isotonic fluid excess

Excessive NS
Hypersecretion of aldosterone which leads
to retention of Na & water
Corticosteroids

Hypertonic Alterations

Osmolality becomes elevated

Causes
Hypernatremia (Na >147 mEq/L)

Rarely occurs with dietary Na

Occurs most often with hypertonic NS (NaHCO3)
Hypersecretion of aldosterone (Cushing syndrome)
Will cause osmotic water attraction

Deficit in ECF water

Fever, respiratory infections (increased RR)

DI, DM, polyuria, profuse sweating & diarrhea
Insufficient water intake
Will cause hypovolemia

Hypernatremia

Clinical Problems

Thirst
Fever
Dry mucous membranes
Restlessness
CNS twitching
Hyperreflexia
Convulsions & pulmonary edema are late
problems if untreated
Will see concentrated urine & S & S of
hypovolemia with water deficits

Hypotonic Alterations

Osmolality is deceased (Na < 135mEq/L)

Causes
Extrarenal losses

Vomiting, diarrhea, GI suction, burns or diuretics

Inadequate Na intake is rare but possible with

diuretics
Dilutional

Hypotonic IVs
Large water intake
Impaired water excretion
Osmotic shifts

Kidney failure to excrete water

Hyponatremia

Clinical Problems

Lethargy
Confusion
Apprehension
Depressed reflexes
Seizures
Coma
Will see hypovolemia S & S with Na loss
Will see weight gain & JVD with dilutional

Water Excess

Compulsive water drinking

Decreased urine formation
Syndrome of inappropriate ADH
(SIADH)
ADH secretion in the absence of
hypovolemia or hyperosmolality
Hyponatremia with hypervolemia

Water Excess (contd)

Manifestations: cerebral edema (with

confusion and convulsions),
weakness, muscle twitching, nausea,
headache, and weight gain

Potassium

Major intracellular electrolyte

Essential for normal cell function
98% intracellular
Regulated by kidney concentration gradients
Not as effective as Na regulation

Essential for transmission and conduction of

nerve impulses, normal cardiac rhythms, and
skeletal and smooth muscle contraction
Insulin & epinephrine promotes intracellular
movement

Hypokalemia

K is < 3.5mEq/L
Generally a low serum K means total K
depletion
Causes

Alkalosis causes K shift into cells to release H

ICF K may be depleted in DKA due to H shifts
Dietary deficiencies are rare
Losses occur through GI or renal disorders

Na loss may cause increased aldosterone production.

Magnesium deficits

Increase renin & aldosterone

Some antibiotics are K wasting

Hypokalemia

Clinical Problems
None if mild
Decreased neuromuscular excitability

Muscle weakness & cardiac dysrhythmias

Progresses from large to smaller muscles
Paralysis & respiratory arrest if untreated

Loss of smooth muscle tone

EKG Effects

Delayed ventricular repolarization

Bradycardia, AV blocks & PAT
Peaked P waves & ST depression

Depressed insulin secretion & glycogen synthesis

Polyuria secondary to inability to concentrate urine

Hyperkalemia

K is > 5.5 mEq/L

Rare because of renal excretion
Causes
Increased intake

Whole blood, IV K & IV Pen G

Cell trauma, burns

Cell membrane permeability changes
Acidosis
Cell hypoxia
Acidosis
Decreased renal excretion
K sparing diuretics

Hyperkalemia

Clinical Problems
Vary with severity
Neuromuscular

Restlessness, intestinal cramping & diarrhea progressing to

weakness , muscle tone loss & paralysis

EKG Effects

Increased resting membrane potential

More rapid repolarization increased cardiac excitability
Narrow & taller T waves, shortened ST segments early
Progresses to depressed ST, prolonged PR & widened QRS
leading V fib & arrest

Increase Ca can override neuromuscular effects

Cardiac Effects of K

Potassium Levels

Changes in pH affect K+ balance

Hydrogen ions accumulate in the ICF
during states of acidosis; K+ shifts out to
maintain a balance of cations across the
membrane; result is hyperkalemia

Aldosterone, insulin, and

catecholamines influence serum
potassium levels
Potassium adaptation
Slow changes tolerated better than acute

Calcium

99% of calcium is located in the

bone as hydroxyapatite
Necessary for structure of bones
and teeth, blood clotting,
hormone secretion, and cell
receptor function
Plasma concentration 9 to 10.5
mg/dL

Phosphate

Like calcium, most phosphate is

also located in the bone
Necessary for high-energy bonds
located in creatine phosphate
and ATP and acts as an anion
buffer

Calcium and Phosphate

Calcium and phosphate

concentrations are rigidly
controlled
Ca++ x HPO4 = K+ (constant)
If the concentration of one
increases, that of the other
decreases

Plasma concentration 2.5 to 4.5

mg/dL

Hypocalcemia

Causes:
Inadequate intestinal absorption, deposition of
ionized calcium into bone or soft tissue, blood
administration
Decreases in PTH and vitamin D
Nutritional deficiencies occur with inadequate
sources of dairy products or green leafy vegetables

Effects:
Increased neuromuscular excitability

Tingling, muscle spasm (particularly in hands, feet,

and facial muscles), intestinal cramping, hyperactive
bowel sounds

Severe cases show convulsions and tetany

Prolonged QT interval, cardiac arrest

Hypercalcemia

Causes:

(contd)

Hyperparathyroidism
Bone metastases with calcium resorption from breast,
prostate, renal, and cervical cancer
Sarcoidosis
Excess vitamin D
Many tumors that produce PTH

Effects:

Many nonspecific: fatigue, weakness, lethargy,

anorexia, nausea, constipation
Impaired renal function, kidney stones
Dysrhythmias, bradycardia, cardiac arrest
Bone pain, osteoporosis

Phosphate

Like calcium, most phosphate is also

located in the bone
Necessary for high-energy bonds
located in creatine phosphate and
ATP and acts as an anion buffer

Hypophosphatemia

Causes:
Intestinal
malabsorption
(vitamin D deficiency,
use of magnesiumand aluminumcontaining antacids,
long-term alcohol
abuse);
Malabsorption
syndromes
Respiratory alkalosis
Increased renal
excretion of
phosphate associated
with
hyperparathyroidism

Effects:

Reduced capacity for

oxygen transport by red
blood cells thus disturbed
energy metabolism
Leukocyte and platelet
dysfunction
Deranged nerve and muscle
function
In severe cases, irritability,
confusion, numbness,
coma, convulsions, possibly
respiratory failure,
cardiomyopathies, bone
resorption

Hyperphosphatemia (contd)

Causes:
Acute or chronic renal
failure with significant
loss of glomerular
filtration
Treatment of
metastatic tumors
with chemotherapy
that releases large
amounts of phosphate
into serum
Long-term use of
laxatives or enemas
containing phosphates
Hypoparathyroidism

Effects:

Symptoms primarily
related to low serum
calcium levels (caused
by high phosphate
levels) similar to the
results of hypocalcemia
When prolonged,
calcification of soft
tissues in lungs,
kidneys, joints

Magnesium

Intracellular cation
Plasma concentration is 1.8 to 2.4
mEq/L
Acts as a cofactor in intracellular
enzymatic reactions
Increases neuromuscular
excitability

Hypomagnesemia

Causes:
Malnutrition,
Malabsorption
syndromes
Alcoholism
Urinary losses
(renal tubular
dysfunction,
loop diuretics)

Effects:

Behavioral
changes
Irritability
Increased reflexes
Muscle cramps
Ataxia
Nystagmus
Tetany
Convulsions
Tachycardia
Hypotension

Hypermagnesemia

Causes:
Usually renal insufficiency or failure
Also excessive intake of magnesium-containing antacids
Adrenal insufficiency

Effects:

Skeletal smooth muscle contraction

Excess nerve function
Loss of deep tendon reflexes
Nausea and vomiting
Muscle weakness
Hypotension
Bradycardia
Respiratory distress

Acid-Base Balance

Acid-base balance is carefully

regulated to maintain a normal PH
via multiple mechanisms

pH (contd)

The pH scale ranges from 0 to

14: 0 is very acidic, 14 is very
alkaline
Each number represents a factor
of 10
If a solution moves from a pH of 6
to a pH of 5, the H+ have increased
10 times

pH (contd)

Acids are formed as end products of

protein, carbohydrate, and fat
metabolism
To maintain the bodys normal pH
(7.35-7.45), the H+ must be
neutralized or excreted
The bones, lungs, and kidneys are
the major organs involved in the
regulation of acid and base balance

pH (contd)

Body acids exist in two forms:

Volatile

H2CO3 (can be eliminated as CO2 gas)

Nonvolatile

Sulfuric, phosphoric, and other

organic acids
Eliminated by the renal tubules with
the regulation of HCO3

Hydrogen & pH

Decreased pH means higher H

concentrations

If the H+ are high in number, the pH is low

(acidic). If the H+ are low in number, the pH is
high (alkaline).

Normal body pH range is 7.35 to 7.45

Body acids are formed as metabolism end
products
Lungs, kidneys & bones work together to
regulate acid base balance
Lungs excrete weak volatile acids H2CO3
(carbonic acid)+ enzyme = CO2 & H2O
Kidneys excrete strong non-volatile acids
(phosphoric & sulfuric)

Buffer Systems

A buffer is a chemical that can bind

excessive H+ or OH without a
significant change in pH
Respiratory & kidney system are
effective together as the carbonic
acid bicarbonate system
Lungs can adjust rate rapidly & kidneys
can adjust urine pH easily

Buffering Systems

A buffer is a chemical that can

bind excessive H+ or OH without a
significant change in pH
A buffering pair consists of a weak
acid and its conjugate base
The most important plasma
buffering systems are the carbonic
acid-bicarbonate pair
CO2+ H2O <>H2CO3<>H + HCO3

Carbonic Acid-Bicarbonate Pair

Operates in the lung and the

kidney
The greater the partial pressure of
carbon dioxide, the more carbonic
acid is formed
At a pH of 7.4, the ratio of
bicarbonate to carbonic acid is 20:1
Bicarbonate and carbonic acid can
increase or decrease, but the ratio
must be maintained

Carbonic AcidBicarbonate Pair

(contd)

The respiratory system

compensates by increasing
ventilation to expire carbon
dioxide or by decreasing
ventilation to retain carbon
dioxide
The renal system compensates
by producing acidic or alkaline
urine

Other Buffering Systems

Protein buffering (hemoglobin)

Proteins have negative charges, so
they can serve as buffers for H+

Renal buffering
Secretion of H+ in the urine and
reabsorption of HCO3

Ion exchange (between ICF and

ECF)
Exchange of K+ for H+ in acidosis and
alkalosis

Carbonic Acid-Bicarb Buffering

Other Buffering Systems

Protein buffering
Proteins have negative charges, so
they can serve as buffers for H+

Renal buffering
Secretion of H+ in the urine and
reabsorption of HCO3

Cellular ion exchange

Exchange of K+ for H+ in acidosis
and alkalosis

Acid-Base Imbalances

Normal arterial blood pH

7.35 to 7.45
Obtained by arterial blood gas (ABG)
sampling

Acidosis

Systemic increase in H+ concentration

or decrease in bicarbonate

Alkalosis

Systemic decrease in H+
concentration or increase in
bicarbonate

Acidosis and Alkalosis

Four categories of acid-base

imbalances
Respiratory acidosiselevation of
pCO2 as a result of ventilation
depression
Respiratory alkalosisdepression
of pCO2 as a result of alveolar
hyperventilation

Acidosis and Alkalosis

Four categories of acid-base

imbalances
Metabolic acidosisdepression of
HCO3 or an increase in
noncarbonic acids
Metabolic alkalosiselevation of
HCO3 usually caused by an
excessive loss of metabolic acids

Respiratory Acidosis

Respiratory Alkalosis

Metabolic Acidosis

Metabolic Alkalosis

Davenport Diagram

Clinical Problems Seen in

Acid/Base Imbalances

Clinical Problems in
Metabolic Acidosis
H/A, lethargy, Kussmaul
respiration, anorexia, N/V,
abdominal discomfort
Leads to coma & death
Clinical Problems in
Respiratory Acidosis
Restlessness,
disorientation, muscle
twitching, tremors, warm
skin due to vasodilation
Rapid RR leading to
depression

Clinical Problems in
Metabolic Alkalosis
Weakness, cramps,
hyperactive reflexes,
tetany, shallow/slow RR,
confusion, convulsions,
atrial tach
Clinical Problems in
Respiratory Alkalosis
Dizziness, confusion,
tingling in extremities,
convulsions & coma
Reduced cerebral blood
flow due to
vasoconstriction

1. Which of the statements is TRUE regarding

water balance?
A. Isotonic fluids cause increased cellular swelling.
B. Hypertonic fluid causes increased cellular
swelling.
C. Hypotonic fluid causes cellular swelling.
D. Hypernatremia causes cellular swelling.

Case Study

A 50 yo F was brought to an urgent

care facility c/o weakness & loose
stools for 2 weeks. The chemstat
machine gives the following values:
Na 142mEq/l, K 2.1 mEq/l, Cl 94
mEq/l & CO2 30 mEq/l.
What lytes are abnormal?
Is there an emergency?
What should be done?