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Nk abg basics
1. Basics for ABG analysis
PROF. N.KRISHNAN
Prof of Anaesthesiology
Madras Medical College
Chief Anaesthesiologist
Institute of Child Health & Hospital for Children
chennai
2. Arterial Blood gas analysis is important
Adequacy of oxygenation
Adequacy of ventilation
Acid base status
3. Acid base balance
ā¢ It is a regulatory process ,whose aim is to maintain optimal
H+ ion conc for bodyās metabolic processes
ā¢ Biochemical and enzymatic processes of cellular
mechanism depends on hydrogen activity.
4. Changes in Hydrogen ions conc
CAN PRODUCE CHANGES IN
Enzyme systems
Electro physiology of myocardium and CNS
Electrolyte balance
Response to exogenous drugs
Alteration in blood flow to organs
5. H+ ion activity
It reflects a balance between production and excretion of acids
Normal value is 40 nanomoles/ liter
(40 x 10-9 ) moles / liter.
It yields a pH of 7.40.
6.
7. Ion
ā¢ Atoms give up, accept or share
electrons with other atoms to
produce an ion
ā¢ Atoms gaining an electron is called
an
ā¢ An i on ā ve
ā¢ Atom which loses an electron is a
ā¢ Ca t ion +Ve.
11. ā¢ Intra cellular Aerobic
Metabolism of
carbohydrates ,fat and
protein yields
ā¢ VOLATILE ACID ( C02)
ā¢ Anaerobic Metabolism, of
carbohydrates, fat and
protein yields
ā¢ NON VOLATILE
ACIDS ( lactic acid)
12. Common Metabolic acids in the body
ā¢ Phosphoric acid from ingested food
ā¢ Sulphuric acid from metabolism
ā¢ Carbonic acid from Co2
ā¢ Beta hydroxyl butric acid
ā¢ Acetoacetic acid
ā¢ Lactic acid.
14. FATE OF ACID
ā¢ DILUTION
ā¢ EXTRA CELLULAR :Rapid process
ā¢ INTRA CELLULAR : Slow process.
15. FATE OF ACID
ā¢ Buffers in blood
ā¢ H+ combines with buffer base
ā¢ H+ exchanges with cellular
cation like Na ,K
ā¢ H+ Exchanges with Ca in bone
22. Bone
ā¢ Bone can take up H+ in exchange for Ca++, Na+ and K+ (ionic exchange) .
Bone can release HCO3
-, CO3
- or HPO4
-2.
ā¢ In acute metabolic acidosis uptake of H+ by bone in exchange for
Na+ and K+ is involved in buffering as this can occur rapidly without any
bone breakdown.
23. Bone
ā¢ In chronic metabolic acidosis, the major buffering mechanism by far is
release of calcium carbonate from bone. The mechanism by which this
dissolution of bone crystal occurs involves two processes:
ā¢ Direct physicochemical breakdown of crystals in response to [H+]
ā¢ Osteoclastic reabsorption of bone.
24. FATE OF ACID- Respiration
ā¢ Fall in pH stimulates chemoreceptors
ā¢ Increase in ventilation
ā¢ Leads to drop in pco2.
25. FATE OF ACID - Kidneys
ā¢ Kidneys maintain acid base balance
ā¢ Slow process
Excretion of H+ IONS
Generation of New HCo3
Reclamation of filtered HCo3
27. Acid excretion by kidneys
PCT
H+ is produced in the tubular cell in the presence of
CARBNIC ANHYDRASE enzyme ,
.
28. Acid excretion by kidneys
DCT & CT
H+ produced is secreted in to lumen of the tubule
ACTIVE ATP DRIVEN PUMPS CALLED PROTON PUMPS .
29. Reclamation of filtered HCo3
In PCT
filtered HCo3 combines with H+ which is secreted from the tubular cell
in exchange for sodium to form H2Co3
30. Generation of new HC03
In DCT via H2Po4 / HPo4 mechanism
Limited to the supply of dibasic phosphate.
HPO4 Combine with H+ to becomes H2PO4 &
1 H+ IS LOST
Na2HPO4
Dissociates
into
2 Na & HPO4
31. Metabolism of amino acid GLUTAMINE in PCT
ā¢ The generates 2 NH+
4
within the tubular cells
and two HCO-
3 ions,
which are then returned
to the systemic
circulation
Glutamine is converted to 2 mole of NH4 and 2 moles of
HCo3
33. Three mechanisms act to excrete this excess amount of H+
from lumen.
1.The number of proton pump in membrane increases
2.Phosphate mechanism
3.Ammonia mechanism .
34. Both Generation and Reclamation of HCo3 is regulated
ā¢Blood pH
ā¢Serum HCo3
ā¢GFR
ā¢Filtered load of HCo3
ā¢PCo2
ā¢Renin / Angio / Aldosterone Mechanism
ā¢K load
38. H+ ion activity
It reflects a balance between production and
excretion of acids
Normal value is 40 nanomoles/ liter
(40 x 10e-9) moles / liter.
It yields a pH of 7.40.
39. pH
pH is the negative logarithm to base 10 of the
hydrogen ion concentration in nanomoles per liter
The raise in pH indicates a proportionate fall in hydrogen
ion concentration and vice versa.
40. pK
pK represents the pH value at which the solute is 50% dissociated
It represents the pH value at which maximum buffering can be achieved.
41. Buffer
Buffer is a substance that resists changes in pH
( hydrogen concentration) by undergoing a
reversible reaction.
A buffer system consists of a weak acid with its strong base or salt.
42. HCo3 buffer
H2Co3 (acid) and NaHCo3 (Salt)
If HCl is added
HCl + NaHCO3 produces H2Co3 + NaCl
H2Co3 is a weak acid compared to the added strong HCL
43. Itās a weak but powerful buffer because
ļ¼High solubility of Co2
ļ¼Presence of Carbonic anhydrase enzymes in RBC and renal tubular
cells.
ļ¼The ability of kidney to synthesize new bicarbonate
ļ¼Efficient removal of carbon dioxide by lung
HCo3 buffer
44. Henderson Hasselbach Equation 1
It expresses acid base relationship by
looking at one component of the
body buffer system
H2Co3 ā H+ + HCo3- (.1)
45. H2Co3 ā H+ + HCo3-
ā¢ HH-2
ā¢ Law of mass action
ā¢ āstates that product of the concentration of
the substance on the right
ā¢ Divided By
ā¢ the concentration of the substance on the
left is equal to a constantā ā Ka
ā¢ H2Co3 ā H+ + HCo3-
ā¢
52. Hco3 [ kidneys ]
pH ----------------------------
pco2 [ lung]
pH is directly related to HCO3.
pH is inversely related to PCO2
53. Buffer Ratio
BASE HCO3- 24
------------- ------------
Acid H2CO3 0.03 X40
Buffer ratio is 20 :1 for HCO3 / H2CO3 BUFFER.
as long as the buffer ratio is maintained the pH will not
change,
even though the amount of hydrogen changes.
54. Key points in H-H Equations
ā¢ pH is Directly related to HCO3
ā¢ pH is Inversely related to pCO2
ā¢ The Ratio of HCO3 : Pco2 defines the pH .
55. pH : is measured by determining the potential difference between
Ag /Agcl reference cell and Hg /Hgcl test cell separated by a pH
sensitive glass membrane.
Pco2 : one electrode is coated with Teflon and is permeable only to
co2.
56. BG machine measures ONLY Pco2 and pH.
Hco3 , Std Hco3 ,Total Co2 ,Buffer Base, Base Excess
are all calculated from nomograms based on H-H equation in vitro .
57. Plasma Hco3 : measured from serum during electrolyte
investigation
. N = 22 ā 26 meq / L
Std Hco3 : Hco3 of whole blood equilibrated under std
conditions of pco2 and temp . N : 21 ā 25 meq /L.
Tco2 : total co2 = Hco3 + dissolved co2 N =23 ā 27 meq / L .
Whole buffer base is the ā unmeasured ā buffers [amino
acid in proteins ] and plasma Hco3 . N: 45 - 50 meq / L .
58. ANION GAP
ā¢ It measures the
UNMEASURED
ANIONS [A-]
accompanying
non volatile acids.
Whole buffer base is the ā unmeasured ā buffers [amino acid in proteins ] and
plasma Hco3 . N: 45 - 50 meq / L .
59. ANION GAP
ANION GAP
is the calculated difference between
negatively charged (anion)and positively
charged (cation) electrolytes.
= [Na+] ā ([Clā] + [HCO3
ā]) =12 mEq/L
(if using with potassium then 16 )
62. BASE EXCESS
BE is the amount of acid or base needed to return a sample of whole
blood to normal pH 7.4 under standard conditions of Pco2 [40] , Po2
[100] and temp of 37c .
63. Normal BE: + or ā 2 meq / L.
BE quantifies the metabolic component.
+ve BE means alkalosis.
-ve BE means acidosis.
64. ACIDEMIA: [H+] ion conc above normal range of 44
nmol /L & pH < 7.36
ACIDOSIS: a process that would cause acidemia if it
were not compensated.
65. ALKALOSIS : a process that would cause
alkalemia if it were not compensated
ALKALEMIA : [H+] ion conc below normal
range of 36nmol /L & pH > 7.44
66. Normal values
ā¢ Serum pH =7.36-7.44
ā¢ Serum H+ = 40 nEq / L
ā¢ Serum Hco3 = 24 mEq / L
ā¢ Serum Pco2 = 40 mm Hg
69. Types of Acid ā Base disorders
ā¢Primary
ā¢Mixed
70. Primary metabolic disorder
ā¢METABOLIC ACIDOSIS
Is a primary process that causes a fall of HCO3
ā¢METABOLIC ALKALOSIS
Is a primary process that causes a rise of HCO3
71. Primary respiratory disorder
ā¢RESPIRATORY ACIDOSIS
Is a primary process that causes a RISE in Pco2
ā¢RESPIRATORY ALKALOSIS
Is a primary process that causes a FALL in pCO2
72. Types of acid ā base disorders
ā¢Primary- single disorders
ā¢ Met- Acidosis : Reduction Of HCO3-
ā¢ Met- Alkalosis: Increase In HCO3-
ā¢ Resp- Acidosis : Increase In Pco2
ā¢ Resp- Alkalosis : Decrease In Pco2
75. Compensation
ā¢ It is the bodyās response to a pathophysiological
process which produced a change in serum pH .
ā¢ It doesn't return the pH to 7.40
76. Kidney senses the change in pH
Adjusts The Reclamation And Regeneration Of Hco3
COMPENSATION FOR PRIMARY RESPIRATORY DISORDER
77. Kidney
ā¢ In Respiratory Acidosis : High pco2 , low pH
ā¢ [ HIGH ACID}
ā¢ Stimulates Tubular Reclamation & Generation of Hco3
78. Kidney
ā¢ In Respiratory Alkalosis : low pco2 , high pH
ā¢ {LOW ACID}
ā¢ Inhibits tubular Reclamation & Generation of Hco3
79. Brain senses the change in pH
Adjusts the ventilation
Compensation for Primary metabolic disorder
80. In Metabolic Acidosis : pH is low , H+ is high
{ HIGH ACID}
Ventilation is increased to Decrease Pco2
81. In Metabolic Alkalosis: pH is high , H+ is low
{ LOW ACID}
Ventilation is decreased to increase PCO2
83. Use of compensation formulae
The degree to which compensation can occur to a met
or resp process can be calculated using compensation
formulae
Works well in range 7.10 -7.60
Formula gives PREDICTED OR EXPECTED values
84. Use of compensation formula
ā¢ If predicted value doesnāt match measured value [ABG slip ]
ļ¶Two primary disorder
ļ¶Insufficient time to achieve full compensation
85. Formulas for compensation in Metabolic Acidosis
ā¢ EXPECTED FALL IN PCO2 [ Exp PCO2]
WINTERS FORMULA
ā¢ Exp PCO2 = 1.5 [HCO3] + 8 (Ā± 2 )
Resp system tries to expel more CO2 -
COMPENSATES
86. Formulae for compensation in metabolic alkalosis
ā¢ Expected rise of pco2 [exp pco2]
ā¢Exp [ pco2 ] = 0.9 [Hco3] + 16
Resp system tries to expel LESS CO2 - COMPENSATES
87. Formulae for compensation ACUTE respiratory alkalosis
ā¢ Expected fall in HCO3 : [exp HCO3 ]
ā¢ ACUTE [ < 8 hrs ]
ā¢ Every 10 mm fall in pco2 below 40
ā¢ Hco3 decreases by 2 meq / L
ā¢ pH increases by 0.08
KIDNEY TRIES TO LOOSE HCO3
88. Formulae for compensation CHRONIC respiratory alkalosis
ā¢ Expected fall in HCO3 : [exp HCO3 ]
Chronic [ > 24 hrs ]
ā¢ Every 10 mm fall in pco2 below 40
ā¢ Hco3 decreases by 5 meq / L
ā¢ pH increases by 0.03
KIDNEY TRIES TO LOOSE HCO3
89. Formulae for compensation in ACUTErespiratory acidosis
ā¢ Expected rise in HCO3 : [exp HCO3 ]
ā¢ ACUTE [ < 8 hrs ]
ā¢ Every 10 mm rise in pco2 above 40
ā¢ Hco3 increases by 1 meq / L
ļ¶pH decreases by 0.08
Kidney tries to save Hco3
90. Formulae for compensation in CHRONIC respiratory acidosis
ā¢ Expected rise in HCO3 : [exp HCO3 ]
Chronic [ > 24 hrs ]
ā¢ Every 10 mm rise in pco2 above 40
ā¢ Hco3 increases by 4 meq / L
ā¢ pH decreases by 0.03
Kidney tries to save Hco3
91. Respiratory acidosis
If measured pH or Hco3 is LOWER than expected value
[Associated METABOLIC ACIDOSIS ]
If measured pH or Hco3 is Higher than expected value
[Associated METABOLIC ALKALOSIS ]
if both measured and expected values are same
[Pure Primary Respiratory Acidosis ]