Acid Base Balance-Integrated Curriculum

 ACID BASE BALANCE & IMBALANCE
 ACIDOSIS, ALKALOSIS & COMPENSATION

1st yr MBBS- Integrated curriculum
Dr Umer Saeed [MBBS; King Edward Medical College, M.Phil, PhD
Biochemistry, Certificate in Medical Teaching, Certificate in Health
Research]
Powerpoint Templates
Page 1
UHS SYLLABUS- BLOCK-3
1. Discuss the concept of acid base balance
2. Interpret metabolic and respiratory

disorders of acid base balance on the basis
of sign, symptoms and ABG findings
3. Describe the Clinical interpretation of acid

base balance
Page 2
The pH of blood ranges between
7.35 to 7.45
Average pH of blood = 7.40
Page 3
HYDROGEN ION HOMEOSTASIS
About 50-100 mmol of H+ are released
from the cells into ECF each day
Control of H+ balance depends on the
function of LUNGS & KIDNEYS
Page 4
THREE BASIC MECHANISMS OF
H+ ION HOMEOSTASIS
1. H+ can be incorporated into water, occuring
normally during oxidative phosphorylation
Page 5
H+ ION HOMEOSTASIS
2. Buffering of H+ to produce weak acid of the
buffer pair, which causes only a slight change in
the pH
Page 6
Page 7
H+ ION HOMEOSTASIS
3. Excretion of H+ (ELIMINATION OF H+ ions ) from
the body by kidneys & intestines
This mechanism is coupled with generation of
HCO3 ions
Page 8
HCO3 REGENERATION USING H+
ION EXCRETION BY KIDNEYS
Page 9
SUMMARY OF THREE MECHANISMS OF
H+ ION HOMEOSTASIS
1. Incorporation into water
2. Buffering by a buffer pair
3. Elimination of H+ ions
Page 10
ROLE OF LUNGS IN
H+ ION HOMEOSTASIS
•The partial pressure of CO2 (pCO2) in plasma is
about 40 mmHg (5.3 kPa)
•This pCO2 depends on;
• Production of CO2 by tissue metabolism
• And the loss through the pulmonary alveoli
Page 11
EXCHANGE OF O2 & CO2 OCCURS
ACROSS THE RESPIRATORY
MEMBRANE
Page 12
ROLE OF LUNGS IN
H+ ION HOMEOSTASIS
• The rate of respiration, and therefore, the rate
of CO2 elimination is controlled by
chemoreceptors located in the medulla and by
those in the carotid & aortic bodies
• Hypoventilation = (PCO2 increases)
• Hyperventilation = (PCO2 decreases)
Page 13
Page 14
ROLE OF LUNGS IN
H+ ION HOMEOSTASIS
• If PCO2 rises above 40 mmHg, the rate of
respiration increases to eliminate CO2
• Lungs have normally a large reserve capacity
for CO2 elimination
• Diseases of the lungs primarily affect the PCO2
• For example: ASTHMA, COPD, EMPHYSEMA
Page 15
2 MAJOR ROLES OF LUNGS IN
MAINTAINING
ACID BASE BALANCE
Page 16
3 MAJOR ROLES OF KIDNEYS IN
MAINTAINING ACID BASE BALANCE
Page 17
KIDNEYS REGENERATE HCO3, EXCRETE
H+ & BUFFER H+ IONS BY AMMONIA
Page 18
KIDNEYS REGENERATE HCO3 IONS,
WHICH ENTER THE BLOOD
Page 19
ARTERIAL BLOOD GASES
(ABGs)
Page 20
Page 21
HH EQUATION EXPRESSES THE
RATIO OF HCO3:PCO2
pH = 6.1 + log HCO3 / PCO2
Page 22
WHAT IS METABOLIC ACIDOSIS?
• It is acidosis which occurs if there is a fall in
the ratio [HCO3]:PCO2 in the blood
pH = 6.1 + log HCO3 ↓ / PCO2
• Metabolic acidosis → If primary abnormality is the
reduction in HCO3 , then fall in plasma pH is METABOLIC
Page 23
WHAT IS RESPIRATORY
ACIDOSIS?
• Respiratory acidosis → If primary abnormality is the rise
in PCO2, then fall in plasma pH is RESPIRATORY
• pH = 6.1 + log HCO3 / PCO2↑
Page 24
THEREFORE, ACIDOSIS OCCURS
IF;
1. HCO3 decreases↓ OR
2. PCO2 rises↑
pH ↓ = HCO3 ↓ / PCO2↑
Page 25
Page 26
COMPENSATION OF
ACIDOSIS
• In either metabolic or respiratory acidosis, the
ratio of HCO3:PCO2 and, therefore, the pH can be
corrected by a change in the concentration of
the other member of the buffer pair in the same
direction as the primary abnormality
[HCO3] ↓ / PCO2 ↓
Page 27
METABOLIC ACIDOSIS WILL BE
CORRECTED BY LUNGS
• This compensation may be either partial or
complete
• The compensatory change in metabolic
acidosis is a reduction in PCO2
pH = 6.1 + log [HCO3] / PCO2
Page 28
RESPIRATORY ACIDOSIS WILL BE
CORRECTED BY KIDNEYS
• While compensatory change in respiratory
acidosis is a rise in HCO3
pH = 6.1 + log [HCO3] ↑ / PCO2 ↑
Page 29
Page 30
Page 31
METABOLIC ACIDOSIS
• The primary disorder in the bicarbonate buffer
system in metabolic acidosis is a reduction in
HCO3
• This results in a fall in the pH of blood
pH↓ = 6.1 + log [HCO3 ↓] / PCO2
Page 32
CAUSES OF LOW HCO3 IN
METABOLIC ACIDOSIS
1. Increased consumption:
• HCO3 is used in buffering H+ more rapidly that
can be generated by normal homeostatic
mechanisms
HCO3 ↓ / PCO2
Page 33
METABOLIC ACIDOSIS
HCO3 / PCO2
Increased consumption of HCO3 occurs in:
1. Diabetic ketoacidosis (very common scenario in UHS)
2. Lactic acidosis
Page 34
CAUSES OF LOW HCO3
IN METABOLIC ACIDOSIS
3. Impaired aerobic metabolism such
as in circulatory shock & myocardial
infarction (lactate is produced in excess)
4. Drugs: for example high dose of
salicylic acid (aspirin)
Page 35
METABOLIC ACIDOSIS
↓HCO3 / PCO2
5. Ingestion of large amounts of methyl
alcohol (which forms formic acid when
metabolized)
Page 36
METABOLIC ACIDOSIS
6. Increased loss from GIT:
• Loss through urine or GIT more rapidly than
can be generated by normal homeostatic
mechanisms. (diarrhea is a common cause)
HCO3↓ / PCO2
Page 37
METABOLIC ACIDOSIS
• Diarrhea is a common cause of metabolic
acidosis (loss of bicarbonate)
• Vomiting of intestinal contents
HCO3↓ / PCO2
Page 38
METABOLIC ACIDOSIS
7. Impaired production of HCO3:
• There is reduced regeneration of HCO3 by
normal homeostatic mechanisms
HCO3 ↓ / PCO2
Page 39
METABOLIC ACIDOSIS
• Reduced HCO3 regeneration occurs in:
• Renal tubular acidosis (inability to excrete H+
ions or to regenerate HCO3- ions)
• Chroinc renal failure (anions of weak acids
accumulate in body fluids as they are not
excreted by kidneys)
Page 40
METABOLIC ACIDOSIS
• In renal glomerular dysfunction, there is
defective HCO3 regeneration due to reduced
filtration of Na+ ions for exchange with H+ ions
Page 41
SUMMARY OF CAUSES OF METABOLIC
ACIDOSIS (LOW HCO3)
1. Diabetic ketoacidosis (increased consumption of
HCO3)
2. Lactic acidosis (increased consumption of HCO3)
3. Renal failure (decreased HCO3 regeneration)
4. Diarrhea (increased loss from GIT)
5. Drugs (aspirin toxicity) (increased consumption of
HCO3)
Page 42
Page 43
COMPENSATION OF
METABOLIC ACIDOSIS
• For compensation of metabolic acidosis,
respiratory centres respond
•CO2 is eliminated rapidly by increased rate of
respiration
↓HCO3 / ↓PCO2 (pH is now restored)
Page 44
Page 45
Page 46
BIOCHEMICAL FINDINGS IN
METABOLIC ACIDOSIS
• pH is low (less than 7.35, uncompensated) or
may be normal (compensated)
• Plasma HCO3 concentration is always low
• PCO2 is normal (uncompensated), OR low,
(compensatory change)
↓HCO3 / PCO2 (normal) UNCOMPENSATED
Page 47
METABOLIC ACIDOSIS
• Uncompensated: pH low; ↓HCO3 / PCO2 (normal)
•Fully compensated: pH normal ↓HCO3 / PCO2 ↓
Page 48
• A patient in emergency ward is drowsy and disoriented. He has
shallow but rapid breathing. Blood glucose is 435 mg/dl. Urine tests
are positive for ketones
• Blood tests show pH 7.30, HCO3 10 mmol/L (14-20mmol), PCO2
35mmHg (28-40 mmHg)
• Which acid base imbalance is likely present?
a. Metabolic acidosis
b. Respiratory acidosis
c. Metabolic alkalosis
d. Respiratory alkalosis
e. Compensated Metabolic acidosis
Page 49
• A known case of ‘unstable angina’ is brought in ICU ward
with chest pain, sweating and drowsiness. His blood glucose is
155 mg/dl and liver functions are normal. ECG confirms
extensive myocardial infarction
• Blood tests show pH 7.36, HCO3 10 mmol/L (14-20mmol), PCO2
23 mmHg (28-40 mmHg)
• Which acid base imbalance is likely present?
c. Metabolic alkalosis
d. Respiratory alkalosis
Page 50
HOW TO TACKLE THE
SCENARIO?
1. pH (is it acidosis, alkalosis or compensated?)
2. HCO3 (metabolic or not?)
3. PCO2 (respiratory or not?)
4. Then tick the correct answer
Page 51
Page 52
RESPIRATORY ACIDOSIS
• The primary abnormality is: CO2 retention
(PCO2 ↑)
• It is due to impaired alveolar ventilation with a
consequent rise in PCO2 (hypercapnia)
pH↓ = 6.1 + log [HCO3] / PCO2 ↑
Page 53
IMPORTANT CAUSES OF IMPAIRED
VENTILATION (respiratory acidosis)
1. Acute respiratory failure:
. Acute asthmatic attack
. Pneumonia (COVID-19 infection)
•2. Chronic respiratory failure:
• COPD (chronic obstructive pulmonary disease) for
example; chronic bronchitis, emphysema
Page 54
3. Damage to respiratory center:
. Road side accidents (head injuries)
4. Chest wall injuries:
• Multiple fractures of ribs
Page 55
5. Drug poisoning causing depression of
respiratory centers in brain:
. Benzodiazepine drugs over dose (diazepam)
6. Comatosed patients:
• Depression of respiratory centers
Page 56
SUMMARY OF CAUSES OF
1. Asthma, Emphysema, Pneumonia
2. Multiple rib fractures
3. Drugs (benzodiazepines overdose)
4. Comatosed patient
Page 57
Page 58
• pH of blood is low (ACIDOSIS)
• HCO3 normal (uncompensated)
• PCO2 always raised
HCO3 (normal) / PCO2 ↑
Page 59
Page 60
COMPENSATION OF
• Renal tubular cells rapidly generate HCO3 by
increasing the activity of Carbonic Dehydratase
• Activity of both Carbonic Anhydrase and
Glutaminase is increased
• Urine becomes more acidic (NaH2PO4)
• RBCs also respond by generating bicarbonate
ions HCO3 ↑ / PCO2 ↑

Page 61
Page 62
An adult male patient is being treated for acute asthmatic
episode, in emergency department. Patient is nebulized and
following blood tests are performed: Blood pH 7.25, HCO3
levels 20 mmol/L (NR: 12-21 mmol) and PCO2 is 96 mmHg

(NR: 40 mmHg). Blood glucose levels are normal. Which acid
base disorder is most likely present ?
c. Respiratory alkalosis
d. Metabolic alkalosis
Page 63
HOW TO TACKLE THE
SCENARIO?
1. pH (is it acidosis, alkalosis or compensated?)
2. HCO3 (metabolic or not?)
3. PCO2 (respiratory or not?)
4. Then decide for the correct answer
Page 64
After a motor bike accident, a young adult is brought
in emergency department with multiple injuries. On
examination, it is noted that a blunt trauma on his
chest wall has resulted in fractures of 5th, 6th & 7th ribs
His respiratory rate is 9/min. Blood glucose in normal
Which acid base disorder might be present?
e. Compensated Metabolic alkalosis
Page 65
Page 66
ALKALOSIS
• Alkalosis results if there is a rise in the ratio
HCO3: PCO2
• In metabolic alkalosis the primary defect in
bicarbonate buffer system is a rise in HCO3
HCO3↑: PCO2
Page 67
ALKALOSIS
• In respiratory alkalosis the primary defect in
bicarbonate buffer system is a fall in PCO2
HCO3 : PCO2 ↓
• Alkalosis is less common than acidosis
because the primary products of metabolism
are H+ & CO2 and not OH- or HCO3 ions
Page 68
Page 69
COMPENSATION OF ALKALOSIS
• In metabolic alkalosis, there is little
compensatory change in PCO2 (little
compensation occurs)
•In respiratory alkalosis, there is a
compensatory fall in HCO3 (less generation of
HCO3 ions)
Page 70
Page 71
Page 72
METABOLIC ALKALOSIS
• There is a rise in plasma HCO3 concentration
• pH ↑ = 6.1 + log [HCO3] ↑ / PCO2
Page 73
CAUSES OF METABOLIC
ALKALOSIS
1. K+ depletion: there is increased regeneration
of HCO3 by the kidneys
Page 74
CAUSES OF METABOLIC
ALKALOSIS
2. Increased HCO3 regeneration: by the gastric
mucosa, when H+ ions & Cl- ions are lost
because of pyloric stenosis or gastric aspiration
This causes hypochloraemic alkalosis
Page 75
CAUSES OF METABOLIC
ALKALOSIS
3. Excessive HCO3 ingestion/infusion: Ingestion
of large amounts sodium bicarbonate to treat
indigestion or gastritis
Intravenous administration of HCO3 can lead to
metabolic alkalosis
Page 76
CAUSES OF METABOLIC
ALKALOSIS
4. Vomiting of gastric contents: Vomiting of
gastric contents alone, without vomiting of
lower GIT contents causes loss of HCl secreted
by the stomach mucosa. The net result is a loss
of acid from ECF leading to metabolic alkalosis
Page 77
CAUSES OF METABOLIC
ALKALOSIS
5. Excessive Aldosterone secretion:
Excessive aldosterone secretion causes
increased reabsorption of Na+ & secretion of H+
leading to increased loss of H+ from kidney
tubules, causing metabolic alkalosis
Page 78
CAUSES OF METABOLIC
ALKALOSIS
6. Diuretics:
There is increased Na+ reabsorption coupled
with H+ secretion, resulting in increased HCO3
reabsorption, causing increased HCO3
concentration in ECF
Page 79
METABOLIC ALKALOSIS
1. K+ depletion
2. Increased HCO3 regeneration
3. Excessive HCO3 ingestion/infusion
4. Vomiting of gastric contents
5. Excessive Aldosterone secretion
6. Diuretics
Page 80
Page 81
METABOLIC ALKALOSIS
• pH = high (uncompensated)
• HCO3 = high
• PCO2 = normal (uncompensated)
pH↑ = HCO3 ↑ / PCO2 normal
Page 82
Page 83
COMPENSATION OF METABOLIC
ALKALOSIS
• Compensation is relatively inaffective
•Although acidosis stimulates the respiratory
centers, alkalosis cannot depress it sufficiently
to bring the pH back to normal
Page 84
ALKALOSIS
• Respiratory inhibition not only leads to
retention of CO2, (HIGH PCO2), but also causes
hypoxia, which can over-ride the inhibitory
effect of alkalosis on the respiratory centre
Page 85
ALKALOSIS
• Consequently CO2 may not be retained in
adequate amounts to compensate for the rise in
plasma HCO3
Page 86
(Which does’nt
occur)
Page 87
Page 88
Page 89
RESPIRATORY ALKALOSIS
• The primary abnormality in the bicarbonate
buffer system in respiratory alkalosis is a fall in
PCO2
• It is due to increased CO2 elimination by lungs
pH ↑ = 6.1 + log [HCO3] / PCO2 ↓
Page 90
CAUSES OF LOW PCO2
1. Hysterical overbreathing: Which over-rides
the normal respiratory control
2. Raised intracranial pressure: (brain stem
lesions); these stimulate the respiratory drive
Page 91
CAUSES OF LOW PCO2
3. Hypoxia: Which stimulates the respiratory
centres
4. Pulmonary edema/fibrosis:
5. Lobar pneumonia:
6. Salicylates; aspirin toxicity (stimulates
respiratory centers)
Page 92
CAUSES OF LOW PCO2
7. High altitudes: Which increases the rate of
respiration due to low atmospheric PO2, causing
increased expulsion of CO2 by lungs
Page 93
1. Hysterical over-breathing
2. Hypoxia
3. Pulmonary edema/fibrosis
4. Lobar pneumonia
5. Salicylates toxicity
6. High altitudes
Page 94
Page 95
BIOCHEMICAL FINDINGS
• pH always raised (uncompensated)
•HCO3 is normal (uncompensated)
•PCO2 always low
pH↑ = HCO3 Normal / PCO2 ↓
Page 96
Page 97
COMPENSATION OF
• pH = normal (fully compensated)
• HCO3 = normal or low
• PCO2 = low
pH normal = HCO3 ↓ / PCO2 ↓
Page 98
Page 99
After a road side accident, an adult female is brought
in emergency in unconscious state. CT scan reveals
hemorrhage, leading to brainstem injury. Respiratory
rate is 34/min. Which acid base disorder may be
present in this case?
Page 100
WHICH ACID BASE IMBALANCE
WILL BE NORMALLY PRESENT?
• A resident of Hunza valley living at high
mountains with an altitude 7000 meters above
ground level
• On examination, his pulse is 90/min and
respiratory rate is 22/min and hemoglobin 17.1
g/dl
Page 101
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The anion gap is the difference
between primary measured cations
(sodium Na+ and potassium K+) and the
primary measured anions (chloride
Cl- and bicarbonate HCO3-) in serum.
Page 106
Page 107
It is important because an increased anion
gap usually is caused by an increase in
unmeasured anions, and that most commonly
occurs when there is an increase in unmeasured
organic acids: IN ACIDOSIS
Page 108
The most common causes of high anion
gap metabolic acidosis are:
ketoacidosis, lactic acidosis, kidney
failure, alcohol abuse
Page 109
A patient is being evaluated in medical ICU. His
plasma pH is 7.47, HCO3 levels 31 mmol/L (14-21
mmol), PCO2 is 36mmHg (28-40 mmHg)
e. Compensated Metabolic alkalosis
Page 110
During a football match, a player received blunt trauma on
his chest wall, and sustained multiple rib fractures.
He complains of severe pain on breathing, and is brought to
emergency. On examination, he is anxious, marked
tenderness over fracture sites, and has a respiratory rate
10/min
Which acid base disorder might be present?
Powerpoint
e. Compensated Metabolic Templates
alkalosis Page 111
A patient is lying unconscious in a state of shock in
medical ICU. His blood gas analysis was performed
which revealed: pH = 7.35, plasma [HCO3] is 30
mmol/L, plasma PCO2 is 65 mmHg

Which acid base disorder is likely present?
e. Compensated respiratory acidosis
Page 112
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 ACID BASE BALANCE & IMBALANCE

 ACIDOSIS, ALKALOSIS & COMPENSATION

1. Discuss the concept of acid base balance

2. Interpret metabolic and respiratory

3. Describe the Clinical interpretation of acid

About 50-100 mmol of H+ are released

from the cells into ECF each day

Control of H+ balance depends on the

function of LUNGS & KIDNEYS

1. H+ can be incorporated into water, occuring

normally during oxidative phosphorylation

2. Buffering of H+ to produce weak acid of the

buffer pair, which causes only a slight change in

3. Excretion of H+ (ELIMINATION OF H+ ions ) from

the body by kidneys & intestines

This mechanism is coupled with generation of

1. Incorporation into water

2. Buffering by a buffer pair

•The partial pressure of CO2 (pCO2) in plasma is

about 40 mmHg (5.3 kPa)

•This pCO2 depends on;

• Production of CO2 by tissue metabolism

• And the loss through the pulmonary alveoli

• The rate of respiration, and therefore, the rate

of CO2 elimination is controlled by

chemoreceptors located in the medulla and by

those in the carotid & aortic bodies

• Hypoventilation = (PCO2 increases)

• Hyperventilation = (PCO2 decreases)

• If PCO2 rises above 40 mmHg, the rate of

respiration increases to eliminate CO2

• Lungs have normally a large reserve capacity

for CO2 elimination

• Diseases of the lungs primarily affect the PCO2

• For example: ASTHMA, COPD, EMPHYSEMA

pH = 6.1 + log HCO3 / PCO2

• It is acidosis which occurs if there is a fall in

the ratio [HCO3]:PCO2 in the blood

pH = 6.1 + log HCO3 ↓ / PCO2

• Metabolic acidosis → If primary abnormality is the

reduction in HCO3 , then fall in plasma pH is METABOLIC

• Respiratory acidosis → If primary abnormality is the rise

in PCO2, then fall in plasma pH is RESPIRATORY

• pH = 6.1 + log HCO3 / PCO2↑

• In either metabolic or respiratory acidosis, the

ratio of HCO3:PCO2 and, therefore, the pH can be

corrected by a change in the concentration of

the other member of the buffer pair in the same

direction as the primary abnormality

• This compensation may be either partial or

• The compensatory change in metabolic

acidosis is a reduction in PCO2

pH = 6.1 + log [HCO3] / PCO2

• While compensatory change in respiratory

acidosis is a rise in HCO3

pH = 6.1 + log [HCO3] ↑ / PCO2 ↑

• The primary disorder in the bicarbonate buffer