IMPORTANTANCE OF ABG IN LIVER

1. ABG

2. Heparinisation of Syringe
0.05 ml heparin is taken for 1ml of blood
Chhapola et al., Use of liquid heparin for blood gas sampling in pediatric intensive care unit: A comparative study of effects of varying volumes of heparin on
blood gas parameters. Indian J Crit Care Med. 2013 Nov 1;17(6):350.
↑PO2, ↓pH,
↓PCO2
Sample Clotted
Correct Dilution
0.1 ml for 1 ml Blood
0.05 ml for 1 ml Blood
[Hub]
Flushed with
Heparin

3. Modified Allen’s test

4. Positioning of hand

5. Positioning of the Needle
•23-25 gauge needle
•For radial artery sampling the skin is
punctured at 30 – 45 degree
•After withdrawal of syringe firm
pressure should be applied for at least
5 minutes
Dev SP, Hillmer MD, Ferri M. Arterial Puncture for Blood Gas Analysis. N Engl J Med. 2011 Feb 3;364(5):e7.

6. ABG vs. VBG
• Colour
• Pulsatile movement of blood
• Compare SO2 in ABG value with
saturation in Pulse oximeter

7. Is it an arterial Sample?
Variable Arterial Blood Venous Blood
pH
paO2
O2 Saturation
HCo3- 22 to 26 mEq/ L
35 to 45 mmHg
95%
80 to 100 mmHg
7.4 (7.35 to 7.45) 7.36 (7.31 to 7.41)
35 to 40 mmHg
70 to 75%
41 to 51 mmHg
22 to 26mEq/ L
paCo2

9. Introduction
• Acid-Base Equilibrium (ABE) is an important parameter within an organism
that determines the relationship between acids and bases produced daily
by both endogenous (cellular) metabolism and (exogenous) acids and/or
bases taken in through food.
• The acids of the organism are represented as the hydrogen ion (H+), while
the bases by the bicarbonate radical (HCO 3).
• The systems or organs of the body that are involved in the regulation of
ABE are mainly the kidneys and the lungs, but in recent years, it is
increasingly recognized that the liver participates in regulation of ABE, but
not equivalently to the kidneys and lungs.

10. • Acid-base balance is very important for the homeostasis of the body
and almost all the physiological activities depend upon the acid-base
status of the body.
• Acids are constantly produced in the body.
• However, the acid production is balanced by the production of bases
so that the acid-base status of the body is maintained.
Principles of ABE

11. Definitions:
• Acid: is any proton donor (a molecule that releases a
proton H+ in water).
A. Strong acids: HCL.
B. Weak acids: Carbonic acid (H2CO3), Lactic acids and
sodium dihydrogen phosphate (NaH2PO4).

12. • Base: is a proton acceptor (a substance accept H+ often with the
release of hydroxyl (OH-) ions).
A. Strong base: Hydroxyl ion (OH-).
B. Weak base: Bicarbonate (HCO3).
• In practice, the acidotic conditions are common than alkalotic ones,
because the body tends to produce more acid than alkali.

13. • Hydrogen ion (H+) contains only a single proton (positively charged
particle).
• It is the smallest ionic particle, it is highly reactive.
• The normal H+ concentration in the extracellular fluid (ECF) is 38 to
42 nM/L.
• The pH is another term for H+ concentration that is generally used
nowadays instead of ‘hydrogen ion concentration’.
HYDROGEN ION AND pH:

14. • An increase in H+ ion concentration decreases the pH (acidosis) and
a reduction in H+ concentration increases the pH (alkalosis).
• In a healthy person, the pH of the ECF is 7.40 and it varies between 7.35
and 7.45
• The maintenance of acid-base status is very important for homeostasis,
because even a slight change in pH below 7.35 or above 7.45 will cause
serious threats to many physiological functions.

16. REGULATION OF ACID-BASE
BALANCE:
• Two types of acids are produced in the body:
1.Volatile acids.
2.Non-volatile acids.
1. Volatile Acids:
• Volatile acids are derived from CO2.
• Large quantity of CO2 is produced during the metabolism of
carbohydrates and lipids.
• This CO2 is not a threat because it is almost totally removed through
expired air by lungs.

17. • 2. Non-volatile Acids:
• Non-volatile acids are produced during the metabolism of other
nutritive substances such as proteins.
• These acids are real threat to the acid-base status of the body.
• For example, sulfuric acid is produced during the metabolism of sulfur
containing amino acids such as cysteine and metheonine; hydrochloric
acid is produced during the metabolism of lysine, arginine and histidine.
• Fortunately, body is provided with the best regulatory mechanisms to
prevent the hazards of acid production.

18. • The body has three different mechanisms to regulate acid-
base status:
1. Acid-base buffer system, which binds free H+
2. Respiratory mechanism, which eliminates CO2
3. Renal mechanism, which excretes H+ and conserves the
bases (HCO3–).
Compensatory Mechanism:

19. • Among the three mechanisms, the acid-base buffer system is the
fastest one and it read justs the pH within seconds.
• The respiratory mechanism does it in minutes.
• Whereas, the renal mechanism is slower and it takes few hours to few
days to bring the pH back to normal.
• However, the renal mechanism is the most powerful mechanism than the
other two in maintaining the acid-base balance of the body fluids.

21. REGULATION OF ACID-BASE
BALANCE BY ACID-BASE
BUFFER SYSTEM:
• An acid-base buffer system is the combination of a
weak acid (protonated substance) and a base – the salt
(unprotonated substance).
• Types of Buffer Systems:
1. Bicarbonate buffer system.
2. Phosphate buffer system.
3. Protein buffer system.

22. Bicarbonate Buffer System:
• Bicarbonate buffer system is present in ECF (plasma).
• HCO3 – is in the form of salt, i.e. sodium bicarbonate (NaHCO3).
• Mechanism of action of bicarbonate buffer system:
• HCl + NaHCO3. this action activated when (fall of pH).
• (NaOH) + H2CO3. this action activated when (rise of pH).
• Importance of bicarbonate buffer system:
• Concentration of HCO3 – is regulated by kidney and the
concentration of CO2 is regulated by the respiratory system.

23. Phosphate Buffer System:
• Phosphate buffer system is useful in the intracellular fluid (ICF), in red
blood cells or other cells, as the concentration of phosphate is more in
ICF than in ECF.
• Mechanism of phosphate buffer system:
• HCl + Na2HPO4.
• NaOH + NaH2PO4.
• Importance of phosphate buffer system:
• Phosphate buffer is useful in tubular fluids of kidneys.
• The elements of phosphate buffer inside the red blood cells are in the
form of potassium dihydrogen phosphate (KH2PO4) and dipotassium
hydrogen phosphate (K2HPO4).

24. Protein Buffer System:
• Protein buffer systems are present in the blood; both in the
plasma and erythrocytes.
• Protein buffer systems in plasma:
i. C-terminal carboxyl group, N-terminal amino group and side
chain carboxyl group of glutamic acid.
ii. Side-chain amino group of lysine
iii. Imidazole group of histidine.

25. • Protein buffer system in erythrocytes (Hemoglobin):
• Hemoglobin has about six times more buffering capacity than the plasma
proteins.
• When a hemoglobin molecule becomes deoxygenated in the capillaries, it
easily binds with H+, which are released when CO2 enters the capillaries.

26. REGULATION OF ACID-BASE
BALANCE BY RESPIRATORY
MECHANISM:
• CO2 + H2O → H2CO3 → H+ + HCO3 –.
• Entire reaction is reversed in lungs when CO2 diffuses from
blood into the alveoli of lungs.
• When metabolic activities increase, more amount of CO2 is produced in
the tissues and the concentration of H+ increases as seen above.
• Increased H+ concentration increases the pulmonary ventilation
(hyperventilation) by acting through the chemoreceptors.
• Due to hyperventilation, the excess of CO2 is removed from the
body.

27. REGULATION OF ACID-BASE
BALANCE BY RENAL
MECHANISM:
• Kidney maintains the
acid-base balance of the
body by the secretion of
H+ and by the retention
of HCO3–.

28. RESPIRATORY
ACIDOSIS:
• Respiratory acidosis is the acidosis that is caused by alveolar
hypoventilation.
• During hypoventilation the lungs fail to expel CO2.
• CO2 accumulates in blood where it reacts with water to form carbonic
acid, which is called respiratory acid.
• Carbonic acid dissociates into H+ and HCO3 –.
• The increased H+ concentration in blood leads to decrease in pH and
acidosis.
• Normal partial pressure of CO2 in arterial blood is about 40 mm Hg.
When it increases above 60 mm Hg acidosis occurs.

30. RESPIRATORY
ALKALOSIS:
• Respiratory alkalosis is the alkalosis that is caused by alveolar
hyperventilation.
• Hyperventilation causes excess loss of CO2 from the body.
• Loss of CO2 leads to decreased formation of carbonic acid and
decreased release of H+.
• Decreased H+ concentration increases the pH leading to respiratory
alkalosis.
• When the partial pressure of CO2 in arterial blood decreases
below 20 mm Hg, alkalosis occurs.

32. METABOLIC
ACIDOSIS:
• Metabolic acidosis is the acid-base imbalance characterized by
excess accumulation of organic acids in the body, which is caused by
abnormal metabolic processes.
• Organic acids such as lactic acid, ketoacids and uric acid are
formed by normal metabolism.
• The quantity of these acids increases due to abnormality in the
metabolism.

34. METABOLIC
ALKALOSIS:
• Metabolic alkalosis is the acid-base imbalance caused by loss of
excess H+ resulting in increased HCO3– concentration.
• Some of the endocrine disorders, renal tubular
disorders, etc. cause metabolic disorders leading to loss
of H+.
• It increases HCO3 – and pH in the body leading to
metabolic alkalosis.

36. Acid Base Disorders
Disorder pH [H+] Primary
disturbance
Secondary
response
Metabolic
acidosis
   [HCO3
-]  pCO2
Metabolic
alkalosis
   [HCO3
-]  pCO2
Respiratory
acidosis
   pCO2  [HCO3
-]
Respiratory
alkalosis
   pCO2  [HCO3
-]

37. Liver and ABE
• The liver is involved in the regulation of ABE through four
pathophysiological mechanisms:
• a) Lactic acid metabolism
• b) Albumin homeostasis
• c) Ketogenesis
• d) Urea production

38. • The liver is the main site in the metabolism of lactic acid produced per day
(70%) .
• Lactic acid in the liver is firstly metabolized to pyruvic acid and then
converted to glucose by gluconeogenesis.
• Both the release of lactic acid from the muscles and its metabolism into
glucose is called the Cori cycle.
• This complete process results in the equivalent release of an HCO 3
radical .
Lactic acid metabolism

39. • Lactic acidosis, which is commonly seen in patients admitted to Intensive
Care Units (ICU), is a result of reduced lactic acid degradation from the
site of production, due to tissue hypoxia (reduced perfusion) and is
caused by vasoconstriction which is due to the stimulation of the
sympathetic-adrenergic axis.
• Thus, the non degradation of lactic acid by the muscles, its non-transfer to
the liver, reduced metabolism, and the non-production of bases leads to
the appearance of lactic acidosis.

40. Albumin homeostasis
• Under normal conditions, albumin is considered to belong to the weak
acids.
• Hypoalbuminemia, either from reduced production (liver failure) or from
increased loss (nephrotic syndrome), results in mild metabolic alkalosis,
• Hyperalbuminemia, which occurs mainly in dehydrated conditions, is
accompanied by mild metabolic acidosis.

41. Ketogenesis
• Oxidation of fats in the liver (mitochondria), leads to the production of keto acids
(3-hydroxybutyric and acetoacetic acid) that are broken down into ions of H+ ,
which then are excreted by the kidneys.
• The production and excretion of keto acids is regulated by a reciprocating
mechanism.
• A decrease of the pH (acidic environment) leads to a decrease in the production
of keto acids.
• In situations of starvation or alcoholism, the body's attempt to produce energy
through fat metabolism, leads to the appearance of a severe degree of metabolic
acidosis.

42. Urea production
• In the liver, NH4 is metabolized to urea, which is excreted by the kidneys.
• The conversion of NH4 requires the consumption of an equivalent amount
of strong base [HCO 3 ] .
• Therefore, the production of urea, as an acidification process, plays an
important role in the regulation of ABE

43. Acidifying and alkalinizing factors in hepatic
diseases

44. Alkalinizing factors
• The disorder of ABE in liver diseases which has been identified by both the
usual technical and the physicochemical models is Respiratory Alkalosis
with marked hypocapnia.
• Growing ascites to a significant degree in combination with hepatic
hydrothorax initially causes shortness of breath and hypoxia ,Attempting to
compensate the body leads to shortness of breath and hyperventilation in
the remaining pulmonary parenchyma resulting in hypocapnia.

45. Alkalinizing factors
• Hypoalbuminemia is perhaps the most important factor in the development
of hypoalbuminemic metabolic alkalosis in patients with liver cirrhosis.
• For each decrease of albumin by 1g/dl there is an increase of bases
(HCO 3 by 3.7mEq/L) .
• It should be noted that the reduction of albumin begins in the early stages
of liver cirrhosis due to the reduced intake of protein through food which
alters the metabolism of proteins and amino acids.

46. Acidifying factors
1. Hyponatremia electrolyte disorder in patients with cirrhosis and ascites .
2. Hyponatraemia results from increased reabsorption of H2O by the
kidneys (as it is observed in hepatorenal syndrome), through the
stimulation of the Renin-Angiotensin system as well as the stimulation of
the antidiuretic hormone, due to the reduction of effective circulating
blood volume .
3. Dilution hyponatraemia [free water ion H2O retention (pH=7.00), as
occurs in patients with liver cirrhosis and ascites], acts as an acidifying
factor and consequently leads to acidosis, known as hyponatraemic
acidosis

47. • Another cause of hyperchloremic MAc in patients with cirrhosis is the
diarrhoea (especially in those taking lactulose) accompanied with loss of
HCO 3 and Cl retention, particularly those with hepatic encephalopathy .
• In addition, these patients show type I renal tubular acidosis (inability to
acidify urine, pH>5.3) in a systemic acidosis state .
• This is likely due to reduced outflow which is accompanied by a reduced
release of Na+ in the distal tubule and an inability to excrete H+ and Cl
ions in the corresponding section of the renal tubule

48. ABE and liver diseases
• ICU patients with cirrhosis: In liver cirrhosis, metabolic alkalosis (due to
hypoalbuminemia) coexists with metabolic acidosis (due to dilution and
hyperchloremia) and mainly with respiratory alkalosis (due to hypocapnia),
which are/is compensated with the result that the pH remains relatively
unchanged
• In patients with liver cirrhosis who are admitted to the ICU, the prominent
disorder of ABE is lactic acidity (>1.9-2.0mmol/L) .
• This increase in lactic acid, is due to increased production (tissue
hypotension-hypoxia, suppression of cellular metabolism due to sepsis,
hypercatabolic syndrome and reduced breakdown in the liver, liver
function loss ,hepato-renal syndrome.

51. • Acute liver failure can be caused by extensive burns, acute respiratory
failure, and sepsis .
• In these cases, there is an excessive increase in lactic acid production
mainly from the visceral areas (and from the lungs in the absence of lung
damage) in the context of acute liver dysfunction .
• Characterized by stress hyperlactemia : mass glycolysis induced by
catecholamines and other cytokines that promote cellular glucose uptake
without hypoxia .
• In milder stages of acute liver damage no substantial pH disturbance is
observed since the involved mechanisms (compensatory and non-
compensatory) are balanced, while in more severe stages lactic acidosis
predominates with coexisting respiratory alkalosis.

52. Conclusion :
• Patients with liver cirrhosis have ABE disorders such as Respiratory
Alkalosis (most common), Metabolic Alkalosis, Metabolic Acidosis,
Respiratory Acidosis and mixed disorders (Metabolic Acidosis and
Respiratory Alkalosis).
• In these cases, failure to assess the underlying ABE disorders often results
in the inadequate and incorrect treatment of the patient's condition.
• These patients have increased mortality due to complications in the
function of other organs (multiorgan failure).

53. • THANK YOU

54. Anion Gap Concept
Anion gap= Unmeasured Anions- Unmeasured
Cations
(Normal Anion gap = 10 ± 2)
 For every 1g/dl reduction in plasma albumin concentration the AG
decreases by 2.5
 Corrected AG = Calculated AG + [2.5 × (4 – albumin)]
Increased UA Decreased UC
Ketoacidosis Hypocalcemia
Lactic Acidosis Hypomagnesemia
Renal Failure Hypogammaglobuline
mia
Poisoning by
alcohol,
salicylates
Alkalosis

55. • Intracellular buffering
↑ [H+
] in ECF→ H+
move in cells through
H+
-K+
exchange and K+
move out of cells→
hyperkalemia is resulted in