At the end of this seminar, students should be able to:

1.Identify proper specimen collection for electrolyte analysis.

2.Describe the effect of blood clotting on the serum potassium.
3.Discuss the effect of refrigeration of whole blood on serum potassium concentrations.
4.Describe the role of antidiuretic hormone and aldosterone in electrolyte balance.
5.Describe the mechanism of the renin-angiotensin system.
6.Calculate the serum "anion gap".
7.Discuss causes of an increased and decreased "anion gap".
8.Calculate the serum osmolality from serum sodium, urea-nitrogen, and glucose.
9.Calculate the "osmolal gap".
10.Discuss causes of an increased and decreased serum osmolality.
11.Describe the application of the Henderson-Hasselbalch in maintenance of acid-base balance.
12.List the major clinical causes for electrolyte and acid-base disturbances.
13.Interpret blood gas data in terms of acid-base status.
14.Differentiate acidosis from alkalosis and determine if the primary cause is respiratory or metabolic.
15.Discuss renal compensatory mechanisms for elimination of hydrogen ion in respiratory acidosis and
retention of hydrogen ion in respiratory alkalosis.
16.Discuss pulmonary compensatory mechanisms operative in metabolic acidosis and metabolic alkalosis.
17.Discuss the criteria for determining renal compensation in chronic respiratory acidosis and chronic
respiratory alkalosis.
18.Discuss the criteria for determining pulmonary compensation in metabolic acidosis and in metabolic
alkalosis.
19.List the major causes of increased and decreased serum bicarbonate, chloride, sodium, and potassium.
 Electrolytes are positively ( cations )and
negatively ( anions ) charged molecules called
ions, that are found within the body's cells and
extracellular fluids, including blood plasma

The intracellular space (ICS) contains a high

potassium K ( cation ) , phosphate HPO3 (anion )
concentration.
While the extracellular space (ECS ) contains a
high sodium Na ( cation ) , chloride Cl ( anion )
concentration.
 SAMPLE COLLECTION FOR
ELECTROLYTE ANALYSIS
Plasma: Ammonium heparinate is the
preferred anticoagulant.

Serum: Potassium values are slightly higher in

serum than in plasma because of release of
potassium from platelets during clotting.
In this condition, plasma potassium rather
than serum potassium should be used.
 The normal potassium level in the blood is
3.5-5.0 milliequivalents per liter (mEq/L)

The increase in potassium concentration due

to clotting depends on the potassium
concentration in the platelets and the
percentage of that potassium released from
the platelets during clotting.

5
 Factors affect the serum potassium

Insulin stimulates the uptake of potassium

into cells
Dehydration can move K+ from the cells to the
blood
Hyperglycaemia can also move K+ out of the
cells

7
 pseudohyperkalemia
Long storage of whole blood specimens
results in release of potassium from
leukocytes and erythrocytes.
Refrigeration of the clotted sample will result
in elevation of serum potassium and
depression of serum sodium due to inhibition
of the Na/K-ATPase pump.
Use of potassium EDTA anticoagulation.
HORMONES IMPORTANT IN ELECTROLYTE
AND ACID-BASE BALANCE

ADH (Vasopressin)
Aldosterone
Renin-Angiotensin System
ADH (Vasopressin)
Produced in hypothalamus, stored in pituitary
Causes water to be reabsorbed by collecting
ducts and ascending loop
Release regulated by osmolality
Diabetes insipidus
Hypothalamic / pituitary: lack of production /
storage
Nephrogenic: kidneys do not respond to ADH
 Role Of ADH And Aldosterone
Hormones In Electrolyte Balance
ADH (VASOPRESSIN) : sodium re-absorption in
exchange of potassium secretion

increase in ADH level in plasma which causes

maximum urine concentration.

decreased the secretion of the ADH

Diabetes incipidus
11
Renin-Angiotensin-Aldosteron System
Angiotensin:
Effect on aldosterone.
Constriction of blood vessels.

Aldosteron:
Increase sodium re-absorption in exchange of
potassium secretion.
Released by angiotensin II.
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Aldosterone
Promotes retention of Na+ and HCO3- and excretion of K+ and
H+ with retention of water
Promotes retention of Na+ and Cl- from sweat gland
Released by angiotensin II (renin released due to decreased
renal perfusion and hyponatremia)
Addisons disease - destruction of adrenal cortex leading to
deficit of aldosterone and cortisol
Conns syndrome (primary hyperaldosteronism: bilateral
hypertrophy of zona glomerulosa; adrenal adenoma; adrenal
carcinoma) - high serum aldosterone leading to low serum
renin
Secondary hyperaldosteronism (hepatic cirrhosis, congestive
heart failure, nephrosis) - high serum renin leading to high
serum aldosterone
 ANION GAP (AG)
The difference between the measured cations
(Na+& K+)and the measured anions (Cl- & HCO3-)
in serum, plasma, or urine.

AG = [Na+] ([Cl] + [HCO3]) = 12 mEq/L

Normal AG IS 12 mEq/L

15
 ANION GAP (AG)
Causes of decreased AG:
Hypoalbuminemia
Hemorrhage
nephrotic syndrome
intestinal obstruction
Hyperlipidemias
Hypercalcaemia and hypermagnesaemia

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 Increase in the AG
A high anion gap indicates acidosis
Ketoacidosis (uncontrolled diabetes, alcoholic,
starvation) caused by acetoacetate and -
hydroxybutyrate (unmeasured anions) .
Renal failure (accumulation of organic acids,
sulfuric acid, phosphoric acid)
Lactic acidosis
 Henderson Hasselbalch equation
describes the derivation of Ph as a measure of acidity
(using pKa, the negative log of the Acid dissociation
constant)

[HA]: weak acid,

[A]:conjugate base
pKa: log10 Ka
Ka: Acid dissociation constant,

18
Based on the equilibria :
CO2 + H2O H2CO3
H2CO3 H+ + HCO3

pH 7.35-7.4
Plasma[H+] (36 - 44) nmol/L
Plasma PCO2 (35-45) mmHg
Plasma [HCO3] (22-26) mEq/L
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 Regulation Mechanism:
1-Buffer system.
Moves or release hydrogen ions

2-Respiratory regulation.
by eliminating or retaining CO2

3-Renal regulation.
Long term regulation of acid-base in body

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 Buffer Systems
1. Protein molecules, phosphate buffer system.
By Removes or release H+ ions.
Acidosis : buffers bind with H+ ions
Alkaline : buffers release H+ ions

2. Bicarbonate-carbonic acid buffer system

by lungs & kidneys to maintain a ratio of 20:1
(bicarb to carbonic acid)

21
22
 2-Respiratory regulation
Eliminates or retains carbon dioxide.
Normal PaCO2 = 35- 45 mmHg

carbon dioxide (acid) stimulate respiration

rate & depth of resp.

Alkalosis depresses respiration

rate & depth of resp retains carbon dioxide

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 3-Renal regulation
Normal bicarbonate 22-26 mEq/L
Acidosis
Excess H+ ions So pH falls
kidneys excrete H+ and retain bicarbonate

Alkalosis
Kidneys retains H+ ions And excrete
bicarbonate

24
 Osmolality
it is the concentration of electolytes in a
sample of blood, urine It is used to evaluate
the balance between water and dissolved
particles in the blood and urine , Normal
values range from 275 to 295 mosm/kg.

Calculated Osmolality =
(Serum Na * 2) + (SerumGlucose/ 18) + (SerumBUN / 2.8)
 Major Clinical Causes of Hyperosmolality:
Dehydration
Hyperglycemia/diabetic ketoacidosis
Diabetes insipidus (serum osmolality high, but urine osmolality low)
Uremia
Ethanol ingestion
Improper specimen collection (use of anticoagulants - this effect is
enhanced in a partially filled tube)
Major Clinical Causes of Hyposmolality:
Overhydration
Inappropriate antidiuretic hormone (ADH) secretion (SIADH) -
serum osmolality low but urine osmolality high
Compulsive water drinking (psychogenic polydipsia)
 Osmolal Gap =
Measured Osmolality - Calculated Osmolality
<10 mosm/kg

A high osmolal gap suggests either the

presence of another compound (e.g., ethanol)
whose identity should be sought, or elevation
of endogenous constituents that may not have
been measured (e.g., proteins, ketoacids).
Acid Base Disorder Diagnosis
STEPS:

1. Look at the pH.

2. Calculate the Anion Gap.
3. Ph and Pco2 direction
Same direction Metabolic
Different direction- Respiratory
4. Apply Winters Formula

28
pH= 7.35-7.45 normal
pH < 7.35 acidosis
pH > 7.45 alkalosis
 Interpreting ABGs

1. Look at the pH

2. Check the CO2 (respiratory indicator)

3. Check the HCO3- (metabolic indicator)

4. Which is primary disorder (Resp. or Metabolic)?

 Compensation

Respiratory system and Renal systems compensate

each other.

pH returns to normal or near normal.

If the non primary system in the normal range then

there is NO compensating.
Ratio of CO2 and HCO3- :
Normal ratio is 1 (CO2) to 20 (HCO3-).
Abnormal ratio creates imbalance.
 1-Metabolic Acidosis
Decrease body pH due to decrease of HCO3-
Most frequent acid-base imbalance.

Cause By :
Diabetes, lactic acidosis = Increase acids
Renal failure = Decrease H+ excretion
Diarrhea = Excessive loss of base
Decreased kidney production of CO3-

35
 Compensatory mechanisms (to lose hydrogen ion):

1. Immediate buffering: HCO3- / H2CO3 buffer

system
2. Respiratory: Hyperventilation; to decrease pCo2
3. Renal phase by;
HCO3- reclamation
Na+ - H+ exchange to increase H+ excretion.
H2PO4- formation & excretion
NH4 production & excretion.

Laboratory findings
HCO3- , pH
After compensation: pCO2 pH will increase to
normal
 2-Metabolic Alkalosis
Increased pH due to accumulation of H2CO3-

Cause By :
prolonged vomiting = Loss of acid from
stomach
Cushings syndrome = loss of K+ and H+ lead
to increased HCO3-
Diuretics Treatment = loss of K+ and H+ ions in
urine, causing increased HCO3-
37
 Metabolic alkalosis
Usually excess accumulation of HCO3 > 26 mEq/L or
loss of acid in body.
Causes :
1. 1- excess vomiting = loss of gastric acid.
2. 2-Cushings syndrome (hyperadrenalism > loss of
K+ and H+, causing increased HCO3-)
3. Excessive ACTH or cortisone (H+ ions are lost in
excess in urine, causing increased HCO3-)
4. Use of diuretics (loss of K+ and H+ ions in urine,
causing increased HCO3-).
5. In hypokalemia, K+ shifts out of cells in exchange for
H+, inducing extracellular alkalosis and intra-cellular
acidosis.
 Compensatory Mechanisms
HCO3- /H2CO3 buffer system.
1. Respiratory by Hypoventilation: causes CO2
retention, increased H2CO3 and decreased pH. Limited
due to hypoxia.
2. Renal phase:
Na+ - H+ exchange, leading to decreased [H+] loss
NH4 production & excretion.
HCO3- reclamation
H2PO4- formation & excretion

Laboratory findings:
HCO3- , pH
After compensation: PCO2 pH will decrease to be
normal
 3-Respiratory acidosis
Decrease body pH due to accumulation of CO2

Cause By :
Prolonged hypoventilation.
CNS depression.
Pulmonary And Cardiac disease.
Severe obesity (interferes with expansion of
the lungs)

40
 Signs and Symptoms of Respiratory
Acidosis
Breathlessness
Restlessness
Lethargy and disorientation
Tremors, convulsions, coma
Respiratory rate rapid, then gradually
depressed
Skin warm and flushed due to vasodilation
caused by excess CO2
 Effect of Acidosis
The main effect of acidosis is depression of the CNS by
in synaptic transmission.
Generalized weakness.
Depressed CNS function.
If acidosis is severe, it causes:
Disorientation.
Coma.
Death.
 Causes of Respiratory Acidosis
Chronic Conditions:
Due to prolonged hypoventilation (CO2 retention, increased
H2CO3, decreased pH).
Depression of respiratory center in brain that controls breathing
rate, e.g., drugs as opiate usage or head trauma.
Paralysis of respiratory or chest muscles.
Pulmonary disease (e.g., emphysema, fibrosis, pulmonary
obstruction)
Cardiac disease.
Acute Conditions:
Pulmonary edema
Pneumothorax
 Compensation for Respiratory Acidosis
Acidosis due to respiratory failure leads to
compensatory renal mechanisms, which lead
to increased reclamation of HCO3- .
Kidneys eliminate H+ and retain HCO3- ion.
Glutaminase enzyme:
Glutamine glutamate + NH3
NH3 + H+ NH4+ (excreted in urine)
Compensatory mechanisms

Renal: Increased HCO3- reabsorption

stimulated by high PaCO2 prevents urinary loss
of bicarbonate.
Metabolic :Reduced production of lactic acid.
Hemoglobin and protein buffer systems

45
 Respiratory alkalosis

Definition: Increase body pH due to deficiency

ofCO2, which does not accompanied by enough
acid to effectively neutralize the effects of alkali.

Cause:
hyperventilation which mean increased rate and
depth of respiration (fever, high external
temperatures, hysteria, anoxia; an early phase of
salicylate poisoning)
 4-Respiratory alkalosis
Increase body pH due to deficiency of CO2

Cause By :
Hyperventilation
Fever
High external temperatures.
salicylate poisoning (early).
Oxygen deficiency at high altitudes
hysteria by Increased rate and depth of respiration

47
By Renal Compensation:
Retention of hydrogen ions.
Excretion of bicarbonate ions.

Compensatory mechanisms (to retain

hydrogen ion)
NH3 production
Na+ - H+ exchange
HCO3- reclamation
H2PO4 formation
Compensatory mechanisms:

1. Renal compensation:
Na+ - H+ exchange
HCO3- reclamation
2. Metabolic compensation by increased
production of lactic and citric acids that react
with and reduce [HCO3-]
49
 Laboratory findings
pCO2 , pH
After compensation: HCO3-

Treatment of Respiratory Alkalosis:

Treat underlying cause.
Breath into a paper bag.
IV Chloride containing solution:
Cl- ions replace lost HCO3- ions.
 Compensatory mechanisms (to lose hydrogen
ion)
1. Hemoglobin and protein buffer systems
2. Hyperventilation
3. Na+ - H+ exchange
4. H2PO4- formation
5. HCO3- retention
6. NH4+ production
Laboratory findings
1. Plasma PaCO2 , pH
2. After compensation HCO3- , tCO2
3. Urine pH
Compensation Calculation

52
 Effect of Alkalosis
Alkalosis causes over excitability of the CNS and
peripheral nervous systems.
Numbness
Lightheadedness
It can cause :
Nervousness
Muscle spasms or tetany
Convulsions
Loss of consciousness
Death
 Salicylate toxicity
Phase 1 characterized by hyperventilation leading
to respiratory alkalosis . last as long as 12 hours.

In phase 2 paradoxical aciduria in the presence of

continued respiratory alkalosis. may last 12-24
hours.

Phase 3 includes dehydration, hypokalemia, and

progressive metabolic acidosis. 24 hours or more
after ingestion in anadult.

55
56
57
 References
Lecture Notes Clinical Biochemistry, Ninth
Edition - Walker, Simon W
Biochemistry Lippincott Illustrated Reviews
Series, 6th Edition
www.Medscape.com (is intended for
healthcare professionals)
Reference :
Clinical biochemistry 9th edition
http://ucsdlabmed.wikidot.com/chapter-
9#toc3
https://books.google.com.sa/books?id=Xs0Yq
SKqAlcC&pg=PA35&dq=normal+range+of+ph+
,+electrolyte&hl=ar&sa=X&ved=0ahUKEwigt5
GM8bDXAhWCwBQKHWPpCKMQ6AEILTAB#v=
onepage&q=normal%20range%20of%20ph%2
0%2C%20electrolyte&f=false
 Q1
Rickys grandmother is suffering from persistent vomiting for
two days now. She appears to be lethargic and weak and
has myalgia. She is noted to have dry mucus membranes
and her capillary refill takes >4 seconds. She is diagnosed as
having gastroenteritis and dehydration. Measurement of
arterial blood gas shows pH 2 85 OaP ,7.5mm Hg, PaCO2
40 mm Hg, and HCO3 34 mmol/L. What acid-base disorder
is shown?

A Respiratory Alkalosis, Uncompensated

B Respiratory Acidosis, Partially Compensated
C Metabolic Alkalosis, Uncompensated
D Metabolic Alkalosis, Partially Compensated
 Q2
Client Z is admitted to the hospital and is to undergo
brain surgery. The client is very anxious and scared of
the upcoming surgery. He begins to hyperventilate and
becomes very dizzy. The client loses consciousness and
the STAT ABGs reveal pH 2 22 OCaP ,7.61mmHg and
HCO3 25 mEq/L. What is the ABG interpretation based
on the findings?
A Metabolic Acidosis, Uncompensated

B Respiratory Alkalosis, Partially Compensated

C Respiratory Alkalosis, Uncompensated

D Metabolic Alkalosis, Partially Compensated