ACID-BASE BALANCE

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 INTRODUCTION
Basic Definitions

Acid-Base Imbalances

Acid-Base Regulations

Disorders of Acid-Base

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 ACID-BASE BALANCE

The mechanisms or processes by which

the body keeps the plasma [H+] constant

Chemical

Physiological

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 pH Review
The acidity or alkalinity of a solution is
measured as pH.

pH = - log [H+]
Range is from 0 14

If [H+] is high, the solution is acidic; pH < 7 i.e.

the more acidic a solution, the lower the pH.

If [H+] is low, the solution is basic or alkaline ;

pH > 7 i.e. the more alkaline a solution , the
higher the pH.
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 The Body & pH
The pH of blood 7.35 - 7.45
7.4 ( optimum pH)
Acidosis <7.35 Alkalosis >7.45
< 6.8 or > 8.0 can result in death

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 WHY ASSESS ACID-BASE
STATUS?
alterations in pH can produce major disturbances:

Enzyme- Optimal activity

Electrolytes- Acid-base balance can also

affect electrolytes (Na+, K+, Cl-)

Protein Denaturation

Hormones - Binding to receptors

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 SOURCES OF ACID LOAD
--- carbonic or volatile acid & non-carbonic or
nonvolatile acids.

Cellular metabolism produces CO2

Acids produced by metabolism of Proteins & Lipids.

Incomplete oxidation of Fats & Carbohydrates.

Acids taken in with foods

Disease processes
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 ACID-BASE REGULATION
The use of buffer systems

The use of the Respiratory

system

The use of the Renal system

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10
BUFFER SYSTEMS

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 BUFFER SYSTEMS
A pH buffer works chemically to
minimize changes in the pH of a
solution

The body uses pH buffers in the blood

to guard against sudden changes in
acidity

Body buffer systems act

instantaneously and constitute the
bodys first line of defense against acid-
base imbalance 12
 BICARBONATE BUFFER

Bicarbonate (HCO3) & carbonic acid

(H2CO3)

It is an important ECF buffer. ~ 75%

Maintain a 20:1 ratio --- HCO3- : H2CO3

H+ + HCO3-H2CO3 CO2+H2O
enz: carbonic anhydrase

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 BICARBONATE BUFFER
H++ HCO3-H2CO3 CO2+H2O
H+ is buffered
Bicarbonate is consumed

Hyperventilation
H2CO3 H2O + CO2
Carbon dioxide diffuses through the
CNS to the respiratory centre and
stimulates hyperventilation

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 BICARBONATE BUFFER
H++ HCO3-H2CO3 CO2+H2O
To stop the backward reaction which
will lead to production of H+ ions, CO2
must be expelled

To generate base from the backward

reaction H+ must be excreted

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 PHOSPHATE BUFFER
Major ICF buffer --~5%
HPO42-/H2PO4-

H+ + HPO42- H2PO4-

Essential in the excretion of acids by

the kidneys.

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 Protein Buffers
~20%
Haemoglobin has a high hydrogen
ion binding capacity effective buffer
in the RBCs

Amino acids have side chains that

can buffer H+ ions
NH2 + H+ NH3+
COO- + H+ COOH
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PHYSIOLOGICAL REGULATION

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 Physiological Buffers
Buffering is but a temporal or
short- term response to
maintaining pH balance.

Eventually all H+ buffered must

be excreted to maintain a normal
pH balance.
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 Physiological Buffers
Serves as the 2nd line of defense.
The 2 main organs primarily
responsible for acid-base regulation
are:

LUNGS- Respiratory regulation

KIDNEY- Renal regulation

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Respiratory Regulation

Respiratory Regulation is
primarily responsible for the
volatile gas- CO

The lungs help regulate acid-

base balance by eliminating
or retaining CO 22
 Respiratory Regulation
Respiratory centers
(Chemoreceptors) in the brain
respondto changes in pH of
blood by altering the rate of
ventilation

The respiratory centers and lungs

are able to regulate the blood pH
by adjusting the speed and depth of
breathing
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 KIDNEY REGULATION OF ACID-
BASE
The kidney regulates acid by 3 main
mechanisms:

Excretion of H

Generation of HCO

Reabsorption of filtered HCO

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 Renal Regulation
With the net effect of eliminating the non-volatile
acid load
A. H+ secretion/excretion
Ammonia buffer
Phosphate buffer

B. HCO3 reabsorption
Proximal tubule 90%
the thick ascending limb & in the collecting
tubule

C. HCO3 Reclamation or regeneration

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Distal tubule
HCO Reabsorption

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HCO REABSORPTION

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HCO GENERATION & H
SECRETION

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HCO GENERATION & H SECRETION

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 ACID-BASE DISORDERS

An acid-base disorder is a change in the

normal pH of the blood that may result
when:

renal or respiratory function is abnormal

acid or base load overwhelms excretory

capacity.

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 Acid-Base Disorders
Acid-Base disorders are divided
into 4 general categories:
Namely:
Respiratory Acidosis
Respiratory Alkalosis
Metabolic Acidosis
Metabolic Alkalosis
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 NORMAL
ACID-BASE VALUES

pH PCO2
HCO3-

Range: 7.35- 7.45 36-

44 22-26

Optimal
value:7.4040
24mmol
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 Acid-Base Disorders
pCO2 is regulated by
respiration, abnormalities
that primarily alter the pCO2
are referred to as respiratory
disorder.

Respiratory acidosis (high

PCO2) & Respiratory alkalosis 36
 Acid-Base Disorders
[HCO3-] is regulated primarily by
renal processes. Abnormalities that
primarily alter the [HCO3-] are
referred to as metabolic disorder.

Metabolic acidosis (low [HCO3-]) and

Metabolic alkalosis (high [HCO3-]).

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 COMPENSATION
When an acid-base imbalance
exists, regulatory mechanisms
occur which attempt to
maintain the arterial pH in the
physiological range.

The normal response of the

respiratory system or kidneys
to change in pH induced by a
primary acid-base disorder is
termed COMPENSATION 38
 COMPENSATION
C o m p l e t e c o m p e n s a t i o n : i f
[ H ] o r p H i s b ro u g h t b a c k w i t h i n
n o rm a l l i m i t s

Pa r t i a l c o m p e n s a t i o n : i f [ H ] o r
p H r a n g e i s s t i l l o u t s i d e re f e re n c e
limit.

Metabolic disorder Respiratory compensation

Respiratory disorder Renal compensation
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 COMPENSATION
Respiratory compensation alteration in
ventilation allows immediate adjustment for
metabolic acid-base disorders

Renal compensation kidneys adapt to

alterations in pH by changing the amount of
HCO3- generated/reabsorbed.

Full renal compensation might take 2-5 days

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 Characteristics of Acid-base disorders
DISORDER PRIMARY RESPONSES COMPENSATORY
RESPONSE

Metabolic [H+] pH HCO3- Increased ventilation

acidosis pCO2

Metabolic [H+] pH HCO3- Decreased ventilation

alkalosis pCO2

Respiratory [H+] pH pCO2 HCO3- H

acidosis Increased renal reabsorption of HCO3-
in the proximal tubule
Increased renal excretion of H + in the
distal tubule

Respiratory [H+] pH pCO2 HCO3- H

alkalosis Decreased renal reabsorption of HCO3-
in the proximal tubule
Decreased renal excretion of H+ in the
distal tubule
 RESPIRATORY ACIDOSIS
Respiratory acidosis is a clinical
disorder characterized by:

a low arterial pH

an elevation in pCO2

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 RESPIRATORY ACIDOSIS
Respiratory acidosis develops when
the lungs does not expel CO2
adequately

Primarily due to hypoventilation

never to increased CO2 production

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 RESPIRATORY ACIDOSIS
Obstruction of air passages
Tracheal cancer

Decreased respiration
(depression of respiratory centers)

Eg. in Drug overdose- eg. Morphine,

opioids, anaesthetics
depresses the respiratory centers
which control breathing rates
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RESPIRATORY ACIDOSIS
Diseases of Lungs Decreased
gas exchange between pulmonary
capillaries & air sacs of lungs.
Emphysema
Bronchitis
Pulmonary oedema
Asthma
CNS disease
meningitis, CNS tumors
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 RESPIRATORY ALKALOSIS
Respiratory Alkalosis is an acid base
disturbance characterized by
elevated arterial pH,
hyperventilation resulting in a low pCO2

Hyperventilation
Leads to eliminating excessive
amounts of CO2
Increased loss of CO2 from the lungs
at a rate faster than it is produced
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RESPIRATORY ALKALOSIS
Psychogenic/psychiatric causes-
Anxiety, hysteria, stress, emotional
disturbances

Anxiety-hyperventilation
syndrome(Psychogenic)

Respiratory center lesions-

Damage to brain centers responsible for
monitoring breathing rates
Eg. Head injury, stroke, tumour
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 RESPIRATORY ALKALOSIS-
DISEASES

Hysterical Overbreathing

Drugs- salicylate poisoning

(overdose)
Hyperventilation is stimulated without
regard to the status of CO2 or H+ in the
body fluids
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 METABOLIC ACIDOSIS
characterized by :
low arterial blood pH
reduced plasma [HCO3-]
An acid-base imbalance not
attributable to CO2

Recognizable by assessing levels of

[HCO3]

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 METABOLIC ACIDOSIS
main causes of metabolic acidosis
are:

Increased endogenous production

Accumulation/decreased excretion
of Acids loads
Increased exogenous acid
administration
Excessive loss of Bases or HCO3-
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 METABOLIC ACIDOSIS
Ingesting an acid/subst. met. into acid
Most substances that cause acidosis
when ingested are considered poisonous
Egs
Methanol to Formate
ethylene glycol (antifreeze) to oxalate
Salicylate to lactate
Aspirin overdose can result in metabolic
acidosis

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 METABOLIC ACIDOSIS
Abnormal Metabolism-
Diabetes Ketoacidosis
Starvation Ketoacidosis

glucose
fat metabolism
Keto acids H+
Acetone, Acetoacetic acid, -
hydroxybutyric acid
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 METABOLIC ACIDOSIS
Lactic acidosis
produced in hypoxic situations-
Respiratory failure, cardiac arrest

Strenuous Exercise
Muscles resort to anaerobic glycolysis
during strenuous exercise
Anaerobic respiration leads to the
production of large amounts of lactic
acid
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 METABOLIC ACIDOSIS
Kidney Insufficiencies

Eg. Renal tubular acidosis or

uremic acidosis may occur in people
with kidney failure or with
abnormalities that affect the kidneys
ability to excrete acid

Proximal renal tubular acidosis

(PRTA; failure to generate or reclaim 54
 METABOLIC ACIDOSIS
Severe Diarrhoea

Fluids rich in HCO3- are released &reabsorbed

during the digestion

In diarrhoea HCO3- is lost from the body rather

than reabsorbed

The loss of HCO3- without a corresponding loss of

H+ lowers the pH

Less HCO3- is available for buffering H+

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METABOLIC ALKALOSIS
characterized by:

an elevation in the arterial pH,

an increase in the plasma [HCO3-]

Increase in pH which has a non-

respiratory origin

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METABOLIC ALKALOSIS
Due to:
A decrease in hydrogen ions or
deficiency of non-carbonic acids

Hydrogen ion loss in the urine or

gastrointestinal tract

the exogenous administration of

bicarbonate
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 METABOLIC ALKALOSIS
Exogenous ingestion of Alkaline Substances
eg. antacids often used as a remedy for gastric
hyperacidity. Sodium bicarbonate, sodium citrate,
gluconate, acetate.
NaHCO3 Na+ and HCO3-

Bicarbonate neutralizes hyperacidity in the

stomach.
The excess bicarbonate is absorbed into the
plasma
increasing pH of plasma.
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 METABOLIC ALKALOSIS
Loss of hydrogen
a. GIT loss: Excessive loss of H+

Removal of gastric secretions:

Eg. Vomiting
. Gastric juices contain large amounts of HCl
. During digestion, HCl secretion, bicarbonate is
also secreted

. During vomiting H+ is lost as HCl and the

bicarbonate is not neutralized in the
plasma
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 METABOLIC ALKALOSIS

Renal loss:
a. Diuretics
inhibit proximal renal reabsorption of
NaCl, leading to an increased load of
sodium to the distal tubule causes
increased H+ secretion and increased
b.HCO3 regeneration.

Mineralocorticoid excess) 60
 ANION GAP
Anion gap- It is the difference
between the sum of the commonly
measured cations and anions in the
plasma or serum calculated as
follows:

([Na+] + [K+]) -([Cl-]+[HCO3-]) =

Anion Gap (AG)

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 ANION GAP
'gap'?- refers to unmeasured anions
The "anion gap" therefore reflects the
concentration of those anions which are actually
present in serum, but are routinely unmeasured.

eg negatively charged proteins (mainly

albumin), phosphates, sulphates and organic
acids lactate, citrate, acetoacetate, etc

If the "anion gap" is bigger than normal, it is

because one of these unmeasured anions is
increased.
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 ANION GAP- IMPTCE
Useful in establishing the cause of
Metabolic acidosis

Metabolic acidosis can be grouped into:

Wide/ High AG
Normal AG
Decreased/ Negative AG

Normal AG= (13- 18 mmol/L)

AG is > 20, its called WIDE AG. 64

WIDE AG METABOLIC ACIDOSIS

Accumulation of organic acids eg.

Lactic acid, Ketones

Toxic Ingestions eg. methanol,

ethylene glycol, salicylates.

CRF- Reduced inorganic acid

excretion or its accumulation eg.
phosphates, sulfates
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Normal AG in Metabolic Acidosis

Diarrhoea- bicarbonate loss & Cl

replacement.

Promixal Renal Tubular Acidosis-

failure to HCO3

Some medications-intoxication with

ammonium chloride.
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ACID-BASE GAS
ANALYSIS

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ACID-BASE GAS ANALYSIS
In the laboratory a patient's acid-base
status is evaluated by a blood-gas
analysis and parameters used are:
Plasma pH

Arterial pCO2

Plasma [HCO]

Anion gap (AG)

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 SAMPLING
Arterial Blood- measure PCO2

Heparinised Blood- prevent coagulation

Sealed Syringe- diffusion of gases from

sample

On Ice- prevent RBC metabolism- lactic

acidosis
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 ABG ANALYSIS -Reference ranges

pH = 7.40 is the optimum pH

(7.35-7.45) is the normal physiological range

PCO = 40 mm Hg (35-45mmHg) ; (5.3kPa) 4.8-5.8 kPa

HCO= (25mmol/L) 21-28 mmol/L

Acidosis: pH < 7.35

Respiratory: PCO > 40 mmHg or > 5.3kPa
Metabolic: HCO <25mmol/L

Alkalosis: pH > 7.45

Respiratory: PCO < 40 mmHg or < 5.3kPa
Metabolic: HCO > 25mmol/L
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 Interpreting ABG analysis
Look at the pH. Determine alkalosis or acidosis
pH < 7.35, acidosis
pH > 7.45, alkalosis
Look at PCO, HCO- determine 1 disorder-
Respiratory or Metabolic
Main pathology will be the change correlates with
the pH.
If alkalosis pCO or Bicarbonate
If acidosis pCO or Bicarbonate
The other abnormal parameter is the compensatory
response
Respiratory or Metabolic
pCO - Respiratory
Bicarbonate - Metabolic 71
 CASE STUDY I
A 23 year old student with type I DM, was rushed
to the KATH with a 1 day history of nausea,
vomiting, polyuria, polydypsia and abdominal
pain and was observed with deep breathing,
orthostatic hypotension, and dry mucous
membranes.

pH =7.27, pCO =23.1mmHg

glucose 7.2, Na=132, K=6.0, Cl=93,
HCO=10mmol/L
U/A: ketones -ve, glucose +ve.

i. Comment on and interpret the biochemical

data. 72
 CASE STUDY II
A 48 year old man was rushed to the
university hospital presenting with 5
days history of vomiting and severe
abdominal pain.

ABG: pH -7.49, PCOmmHg -52,

PO- 78mmHg
Na- 137, K- 2.2, CL -91, HCO-
38mmol/L
Comment on and interpret the
i.
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biochemical data
 MIXED ACIDBASE DISORDER

presence of more than one simple

acid-base disorder simultaneously

eg. A patient with chronic bronchitis

and renal impairment ??

Salicylate poisoning- ?? Respiratory

alkalosis and metabolic acidosis.
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Thank you for your
audience

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 MIXED ACIDBASE DISORDER
Characteristically present in any of the two
following ways:

Severe acidaemia or alkalaemia or a normal or

near normal pH

pH is normal but pCO levels & [HCO] abnormal

The expected compensatory response does not

occur OR
compensatory response occurs, but level of
compensation is inadequate or too extreme.
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