1. Blood gas analysis evaluates respiratory gas exchange, acid-base status, electrolytes, glucose, and osmolality. Significant pH deviations can cause intracellular metabolic issues. 2. The human body tightly regulates pH between 7.35-7.45 through buffer systems, respiration, and the kidneys. The main buffer system involves bicarbonate and carbonic acid, while respiration controls carbon dioxide levels and the kidneys regulate acid excretion. 3. Analyzing arterial blood gases provides information about respiratory and metabolic acid-base disorders. The anion gap and bicarbonate levels indicate the degree and cause of acidosis or alkalosis. Diagnosis involves considering pH, carbon dioxide, and b

1. Blood gas analysis:
acid– base, fluid, and electrolyte
disorders

2. 1 ABG analysis
Evaluation and monitoring of respiratory gas
exchange, acid– base status, basic electrolyte
concentrations (serum [K+], [Na+], [Ca2+]),
plasma glucose, and osmolality
3 Important agents affected pH
changes
Local anaesthetic agents.
Vasopressors.
Inotropes.
Neuromuscular- blocking agents
2 Any significant pH deviation
Intracellular metabolic derangement and
reduced protein synthesis and transport
activity, with significant physiological and
clinical sequelae
4
Prompt diagnosis and
management underlying aetiology
Care should be taken to distinguish respiratory
and metabolic disorders, and acute from
chronic conditions with any physiological
compensation that may have occurred
Blood gas analysis and acid – base disorders

3. Physiological effects of altering pH

4. Maintenance of acid–base balance in the human body
The normal pH range in the human body
is narrow (7.35– 7.45)
H2CO3 is the largest source of hydrogen ions
(H+) in the human body and is a volatile (or
respiratory) acid, dissociates into either H+
ions and bicarbonate ions (HCO3−) or CO2 and
water, with the respiratory acid (CO2)
subsequently being excreted by the lungs
pH homeostasis is maintained, acids
produced by the body must either be
buffered (neutralized) or excreted
The buffer system.
The respiratory system.
The renal system

5. The buffer system
•This is responsible for over 50% of the buffering capacity of the body and is the main
component of ECF buffering (80%).
•When excess H+ ions are added to the systemequilibrium shifts to the leftformation of
H2CO3 by the reaction of H+ ions with HCO3−.
•When H+ ions are removed from the reaction [or excess base added, e.g. hydroxide ions
(OH−)]  equilibrium shifts to the right dissociation of H2CO3 to release H+ ions.
Bicarbonate– carbonic acid buffer
•At the Ph of the human body, the predominant buffer pair is dihydrogen phosphate (H2PO4−)
as the weak acid, and hydrogen phosphate (HPO42– ) as the weak base
•The pKa of H2PO4− is 7.21, making the phosphate buffer system an ideal buffer in the human
body
Phosphate buffer

6. The buffer system
Protein buffers
Protein buffers in blood include both
haemoglobin and plasma proteins
The plasma protein buffering system is the most
abundant intracellular and ECF buffering pair but
is responsible for only 15% of the body’s
buffering capacity
Haemoglobin and
oxyhaemoglobin
CO2 from the cells enters erythrocytes and
combines with water to form H2CO3 by the
action of carbonic anhydrase.
Oxyhaemoglobin gives up its bound O2 to the
cells, producing reduced haemoglobin
(negatively charged).

7. The buffer system
RBC
H2CO3 dissociates into H+ and HCO3−. The HCO3− ions
diffuse into plasma in exchange for chloride (Cl−) ions (the
chloride shift) to retain electroneutrality, and reduced
haemoglobin attracts H+ ions (binding them more readily
than oxyhaemoglobin).
This results in the formation of protonated haemoglobin
(H- Hb), which is a weaker acid than H2CO3
Bohr effect
When blood reaches the pulmonary capillaries, the
presence of a high O2 concentration favours O2 binding
and promotes the loss of H+ ions from H- Hb.
Reduced haemoglobin is converted to oxyhaemoglobin,
and H+ ions are released and buffered by the bicarbonate–
carbonic acid system to form CO2 and water.
Aqueous CO2 follows a concentration gradient into blood,
across the alveolar membrane, and into the alveolar space
where it is eliminated during ventilation

8. The respiratory system
The addition of H+ ions to blood activates the bicarbonate– carbonic acid buffer
system, increasing H2CO3 concentration.
This subsequently dissociates into CO2 and water, and excess CO2 then diffuses
passively into the alveoli of the lungs and is eliminated.
Ventilation plays a major role in pH
homeostasis by eliminating or
conserving CO2.
•Stimulated by free H+ ions, CO2 in plasma, and CO2 in the cerebrospinal fluid,
respectively↑respiratory rate and tidal volume, leading to greater minute
ventilation and increased CO2 elimination
Peripheral chemoreceptors in the
carotid and aortic bodies and
central chemoreceptors in the
medulla oblongata
If the HCO3− concentration is increased (metabolic alkalosis), the CO2 concentration
increases to buffer the excess HCO3− (respiratory compensation).
High HCO3− concentration therefore inhibits central and peripheral chemoreceptors,
resulting in reduced minute ventilation (rate . tidal volume) and reduced CO2
elimination
By controlling CO2 concentration of
blood, the respiratory system is
capable of compensating for pH
changes due to metabolic
derangement.

9. The renal system
Kidneys actively regulate acid– base balance through several mechanisms:
1. Reabsorption of HCO3 − for use in the bicarbonate– carbonic acid buffer system.
2. Excretion of fixed acids [e.g. ammonium (NH4+) and titratable acids] which also results in HCO3
− production
Particularly low urinary pH (high urine acidity) is a good indicator of renal compensation for
systemic acidosis; however, as all mechanisms are via active transportation, compensation is
slow, taking days, rather than minutes.
In response to a low pH, H+ ions are secreted into the urine either in exchange for Na+ ions via the Na+– H+ antiporter or by
using the H+– ATPase active transport systems.
Excess H+ secretion by H+– ATPase pumps in distal convoluted tubular cells, in response to an acid load, leads to greater NH3
diffusion into the tubules and its combination with H+ to form NH4+, and hence greater excretion of free H+ ions. HCO3− is
simultaneously produced in the proximal tubules by the metabolism of α- ketoglutarate and is then transferred to the
systemic circulation

10. Arterial blood gas analysis
Base excess and HCO3−
concentration will inform the
clinician of the degree of acidosis/
alkalosis (with or without Ph
change)
Conversely, ‘base deficit’ defines
the amount of strong base that
must be added to restore normal
pH to blood, assuming the blood
sample is fully oxygenated, at a
temperature of 37°C, and PaCO2
is maintained at 40 mmHg
Basis interpreting acid– base
balance  interdependence
between pH, HCO3−
concentration, and PaCO2
‘standard bicarbonate’ and ‘buffer
base followed by the concept of
‘base excess’ (the concentration of
H+ ions required to return the pH of
blood to 7.4)

11. The H+ ions produced by these acids are buffered by
HCO3−, reducing the concentration of the measured
anions that, in turn, increases the proportion of
these unmeasured anions, and the gap increases.
The predominant unmeasured extracellular cations
are K+, Ca2+, and magnesium (Mg2+), so the AG can
be affected by increases or decreases in unmeasured
cations or anions
Unmeasured anions and cations contributing to the AG
Anion Gap
Formula AG

12. A normal AG is <11 mEq/ L, and a high
gap usually indicates metabolic
acidosis.
Using the AG can help to differentiate
between HCO3− loss and consumption
(e.g. a renal from a non- renal cause of
metabolic acidosis).
An AG acidosis is also present,
regardless of the pH or [HCO3−], when
the AG is >20 mEq/ L
Causes of alterations in the plasma AG

13. Normal AG acidosis results from a net increase in [Cl−],
secondaryto a loss of HCO3−. This is known as
hyperchloraemic metabolic acidosis and is most
commonly associated with:
•GI HCO3− loss (diarrhoea, ileus, pancreatic fistula, villous adenoma).
•Renal HCO3− loss (AKI, proximal and distal renal tubular acidosis,
carbonic anhydrase inhibitors).
•Isotonic (0.9%) saline infusion.
Hypercarbia causes significant physiological changes.
•At low levels, there is generalized cardiovascular, respiratory, and
autonomic stimulation
•An alveolar PACO2 of >100 mmHg is incompatible with life when a
patient is breathing room air, due to associated severe hypoxaemia that
will result from the high partial pressure of CO2 in the alveolus
Physiological effects of hypercarbia by system

14. Acid– base disorders: pathophysiology, compensatory mechanisms,
and common causes

15. Is the pH normal?
•If the pH is <7.35, then
acidaemia is present; if
it is >7.45, alkalaemia
predominates. If it is
normal, there is either
no disturbance or a
compensated or mixed
state exists
Algorithm for initial acid– base interpretation
Normal ABG values

16. •If PaCO2 is altered, the primary disturbance is respiratory.
•If [HCO3−] is altered, the primary disturbance is metabolic.
•If both are abnormal, then the directional change should be compared, which will help to
identify the specific disorder.
•If both PaCO2 and pH change in a direction opposite from each other, the primary
abnormality is respiratory.
•If both PaCO2 and [HCO3−] change in the same direction(either increasing or
decreasing), the primary disorder is metabolic.
•If PaCO2 and [HCO3−] change in the opposite direction, then the primary disorder is
mixed.
•If the trend of change in PaCO2 and [HCO3−] is the same, the one with the greatest
percentage difference from normal is the dominant disorder (as compensation is not
perfect).
Is the primary disturbance respiratory or metabolic?

17. Algorithm for initial acid– base interpretation

18. If the primary disturbance is respiratory, is it acute or chronic?
If PaCO2 is high, it is important to
gauge its chronicity by examining the
ratio between the change in [H+] and
PaCO2 from their reference values
∆H++ ∆PaCO2
Note: >0.8, acute; 0.3– 0.8, acute on
chronic; <0.3, chronic)

19. • Respiratory compensation for metabolic disorders can be marked. This can be investigated using
the Winter’s formula to calculate the expected PaCO2:
• If the actual PaCO2 is the same as the expected PaCO2, then there is adequate respiratory
compensation.
• If the actual PaCO2 is less than the expected PaCO2, then there is concomitant respiratory alkalosis.
• If the actual PaCO2 is more than the expected PaCO2, then there is concomitant respiratory
acidosis.
• In general, respiratory compensation results in a 1.2 mmHg change in PaCO2 for every 1.0 mEq/ L
change in plasma [HCO3−], down to a minimum of 10– 15 mmHg and a maximum PaCO2 of 60
mmHg
If the primary disturbance is metabolic, also calculate the expected PaCO2.

20. If the AG is normal and the cause is
unknown, then calculate the urine
AG (UAG).
This will help to
differentiate renal
tubulopathies from
other causes of non-
elevated AG acidosis.
If UAG is positive:
renal tubular
acidosis or early
acute renal failure
is the likely
diagnosis.
If UAG is negative:
most likely a GI
cause of metabolic
acidosis.
If it is >11 mEq/ L, then the
metabolic acidosis is due
to one of the disorders
noted in E Table 16.4. If it
is normal, then any
metabolic acidosis is likely
to be GI or renal in origin.
If the primary disturbance is
metabolic acidosis, calculate the
AG.

21. THANK YOU
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