Acid base balance and ABG interpretation presented by Dr.Gopan.G,Post-Graduate student. Chairperson : Dr.Ravi.R,Professor, Department of Anaesthesiology & Critical care,JJMMC,Davangere.
2. Over view
1. Basics concepts
2. History ;approaches
3. Acid base disorders ®ulation
4. Treatment
5. interpretation
3. In pure water at 25°C, the [H+] and [OH-] are 1 × 10-7
mmol/L.
A solution is considered acidic if the concentration of
hydrogen ions exceeds that of hydroxyl ions.
A solution is considered alkaline if the hydroxyl ion
concentration exceeds the hydrogen ion concentration.
H2O ↔ H+ + OH-
Basic concepts
Physical Chemistry of Water
4. • pH -the negative logarithm of the hydrogen
ion concentration
• pH for pure water is 7.0
• Physiologic pH, for the ECF, is 7.4, which is
alkaline.
• Henderson Hasselbalch equation :
pH = pK + log [HCO3
-]/αPaCO2
Cont‘d
BASIC CONCEPTS
5. • A substance is an acid if, when added to a
solution, it brings about an increase in the
hydrogen ion concentration of the solution
• A substance is a base if, when added to a
solution, it brings about a decrease in the
hydrogen ion concentration of the solution
Definitions: Acid & Base
6. • Consequently, strong cations—Na+, K+, Ca2+,
Mg2+—act as Arrhenius bases (because they
drive hydroxyl out of, and hydrogen into,
solution, to maintain electric neutrality)
• Strong anions—Cl-, LA-, ketones, sulfate and
formate—act as Arrhenius acids
8. • tools that have evolved over the past 50
years
• None are entirely accurate, and each has a
dedicated group of followers
• Textbooks and clinical practice have tended
to overestimate the importance of isolated
changes in hydrogen or bicarbonate ion
concentration
• Clinical significance of acid-base balance is
determined by the underlying cause, rather
than the serum concentration of hydrogen
and hydroxyl ions
Analytic Tools Used in Acid-Base
Chemistry
10. • Siggard Andersen developed the concept base
deficit/excess
• Base deficit/excess : Defined as the amount
of strong acid or base required to return pH
to 7.4, assuming a PCO2 of 40 mm Hg and
temperature of 38°C
• Current algorithms for computing the
standardized base excess (BE for ECF) are
derived from the Van Slyke equation
• SBE = 0.9287 [HCO3
- - 24.4 + (PH – 7.4)]
• Ref:Miller‘s anesthesia 7th edition Pg:1564
Base Deficit/Excess (Copenhagen)
Approach
11. • proposed ―whole-blood buffer base‖
• The sum of the bicarbonate and the
nonvolatile buffer ions
(serum albumin, phosphate, and hemoglobin)
• [Na+] + [K+] - [Cl-] = 48-49 mmol/L
• Buffer base increases in metabolic alkalosis
and decreases in metabolic acidosis.
Cont‘d
13. • Developed by Emmett and Narins
• Anion gap = [Na+ + K+ - (Cl- + HCO3
-)]
• Sum of the difference in charge of the
common extracellular ions reveals an
unaccounted for ―gap‖ of -10 to -12 mEq/L
• Anion gap is based on the law of electric
neutrality
Anion Gap Approach
15. • Most critically ill patients are
hypoalbuminemic, and many are also
hypophosphatemic
• Consequently, the gap may be normal in the
presence of unmeasured anions
• Anion gap corrected for albumin = calculated
anion gap + 2.5 ( Normal albumin in gm/dL –
observed albumin in gm/dL )
• Second weakness with this approach is the
use of bicarbonate in the equation
Failure of Anion-Gap approach
16. • Electric neutrality
• Dissociation equilibriums
• Mass conservation
Determined the hydrogen ion concentration of
ECF , by applying laws of :
Stewart Approach
17. • Small advance from the ―anion gap‖ approach
• Proposed ―SIG‖
• SIG = Apparent SID –Effective SID(UMA)
• Normal ―SIG‖ is 8 ± 2 mEq/L
• Apparent SID = ([Na+]+ [K+]+ [Mg2+]+
[Ca2+]) - [Cl-])
• Effective SID = [HCO3
-] + [charge on
albumin] + [charge on Pi]
Stewart-Fencl Approach
19. • The strong ion difference (SID)
• The total concentration of weak acids (ATOT).
• The PaCO2
Only three factors independently
affect acid-base balance
20. • ([Na+] – [Cl-]) + ([H+] – [OH-]) = 0
• [H+] = √Kw‘ +([Na+] – [Cl-])2 /4-([Na+] –[Cl-]) /2
• [OH-] = √Kw‘ +([Na+] – [Cl-])2 /4-([Na+] –[Cl-]) /2
• hydrogen and hydroxyl concentrations are
determined by the KW′ and the difference in
charge between sodium and chloride
• Dissociate completely.
• Strong ions in the ECF are
Na+,K+,Mg2+,Ca2+,SO4
2- and Cl-
STRONG ANIONS
21. • The sum total of the charges imparted by strong
cations minus the charges from strong anions.
• SID=([Na+]+[K+]+[Ca2+]+[Mg2+]) – ([Cl-]+[A-])
=40-44 mEq
(1)STRONG ION DIFFERENCE
22. Effect of changes in SID on hydrogen and hydroxyl ion
concentration. ( Can J Physiol Pharmacol 61:1444-
1461, 1983.)
23. • weak acids are partially dissociated
compounds
• Albumin and phosphate
• Stewart used the term ―ATOT‖ to represent the
total concentration of weak anions
(2)Weak Acid ―Buffer‖ Solutions
24. • Exists in four forms: CO2 [dissolved CO2(d)],
carbonic acid (H2CO3), bicarbonate ions
(HCO3
-), and carbonate ions (CO3
2-).
• The concentration of CO2 in ECF is determined
by tissue production and alveolar ventilation.
• As CO2 increases HCO3- also increases.
(3)Carbon Dioxide
25. LAWS EQUATIONS
Water dissociation equilibrium [H+] × [OH-] = Kw‘
Weak acid dissociation equilibrium [H+] × [A-] = KA × [HA]
Conservation of mass for weak
acids
[HA] + [A-] = [ATOT]
Bicarbonate ion formation
equilibrium
[H+] × [HCO3
-] = KC × PCO2
Carbonate ion formation
equilibrium
[H+] × [CO3
2-] = K × [HCO3
-]
Electric neutrality [SID] + [H+] - [HCO3
-] - [A-] -
[CO3
2-] - [OH-] = 0
Stewart combined six derived
equations to solve for [H+]:
26. • [ SID ] + [ H+ ] – KC ×PC/[H+] – KA - [ATOT]/(KA +
[H+]) –K × KCPC/[H+]2 – KW‘/[H+] =0
• [ H+ ] is a function of SID, ATOT, PCO2
• [H+] , [OH-] and [HCO3
-] are dependent and
cannot independently influence acid-base balance
Although the above-listed equations look simple, they
require fourth-order polynomials for solution. This is
impossible without computer technology
27. • Alterations in arterial carbon dioxide (PaCO2)
tension—respiratory acidosis or alkalosis
• Alterations in blood chemistry—metabolic
acidosis or alkalosis.
Acid-Base Abnormalities
Classification
28. Terminology of Acid-Base
Disorders
The definitions of the terms used to describe acid-
base disorders are suggested by the Ad-Hoc
Committee of the New York Academy of Sciences in
1965
Simple (Acid-Base) Disorders are those in which
there is a single primary aetiological acid-base
disorder
Mixed (acid-Base) Disorders are those in which two
or more primary aetiological disorders are present
simultaneously.
29. • neurologic injury (e.g., stroke, spinal cord
injury, botulism, tetanus)
• toxic suppression of the respiratory center
(e.g., opioids, barbiturates, benzodiazepines)
• neuromuscular disorders (e.g., Guillain-Barré
syndrome, myasthenia gravis)
• flail chest, hydro-hemo-pneumothorax,
pulmonary edema, and pneumonia.
Acute respiratory acidosis:
Acid-Base Disturbances in the
Emergency Setting
30. • anxiety, central respiratory stimulation (as
occurs early in salicylate poisoning)
• excessive artificial ventilation
Acute metabolic acidosis
• severe diarrhea,renal tubular acidosis
• Dilutional acidosis
• lactic acidosis, renal acidosis, ketoacidosis
Acute respiratory alkalosis
Cont‘d
32. • hypoalbuminemia (imp)
• metabolic alkalosis that can mask significant lactic
acidemia
• Mechanical ventilation increases the circulating volume
of antidiuretic hormone-dilutional acidosis
• Nasogastric suctioning causes chloride loss, diarrhea
leads to sodium and potassium loss
• Surgical drains placed in tissue beds will remove fluids
with varying electrolyte concentrations
Acid-Base Disturbances in Critical Illness
33. • Respiratory acidosis occurs when there is an
acute increase in PaCO2 principally resulting
from respiratory failure
• Cyanosis, vasodilation, and narcosis
• Respiratory alkalosis occurs when there is an
acute decrease in PaCO2 as a result of
hyperventilation
• Light headedness, visual disturbances,
dizziness, and hypocalcemia
Respiratory Acid-Base
Abnormalities
34. • Associated with alterations in transcellular
ion pumps and increased ionized calcium
• Vasodilation, diminished muscular
performance (particularly myocardial), and
arrhythmias
• Oxyhemoglobin dissociation curve shifts
rightward to increase oxygen offload into the
tissues
Metabolic acidosis
35. • In dysoxia and states of severe stress, lactate
is produced
• In diabetic-ketoacidosis—β-hydroxybutyrate
and acetoacetate—are produced
• In severe renal failure, SO4
2- and PO4
3- (―fixed
renal acids‖) are not excreted, causing
acidosis
• Severe metabolic acidosis is associated with
increased SIG(UMA)
METABOLIC ACIDOSIS
36. • In dilutional & hyperchloremic acidosis
relative ratio of cations to anions
decreases(relative increase of anions).
• In contraction alkalosis relative ratio of
cations to anions increases
• Doberer etal : acidosis develops because of
dilution of HCO3
- (HCO3
- in the blood is
a"closed system") without there being a
dilution of acid in the form of CO2 gas (which
due to its ability to be exhaled can be
considered an "open system").
Dilutional acidosis , hyperchloremic
acidosis and contraction alkalosis
37. • Hypoalbuminemia decreases ATOT, increases
SID and is associated with metabolic
alkalosis.
• SID=([Na+]+[K+]+[Ca2+]+[Mg2+]) – ([Cl-]+[A-])
• The presence of hypoalbuminemia may mask
the detection of acidosis caused by
unmeasured anions
HYPOALBUMINEMIA
38. Abnormalities Acidosis Alkalosis
Respiratory Increased PCO2 Decreased PCO2
Metabolic
Abnormal SID
Caused by water
excess or deficit
Water excess = dilutional Water deficit = contraction
↓ SID +↓[Na+] ↑ SID ↑[Na+]
Caused by
electrolytes
Chloride excess Chloride deficit
Chloride
(measured)
↓ SID ↑[Cl-] ↑ SID +↓[Cl-]
Other
(unmeasured) anions,
such as lactate and
keto acids
↓ SID ↑[UMA-] —
Abnormal ATOT
Albumin [Alb] ↑[Alb] (rare) ↓[Alb]
Phosphate [Pi] ↑[Pi]
Stewart approach for Acid-Base Disturbances
39. • The major source of acid in the body is CO2
• Excreted by the lungs
• Only 20 to 70 mEq of hydrogen ions are
excreted through the kidney each day
• CO2 is buffered directly by hemoglobin and by
plasma proteins
Respiratory failure
Regulation of Acid-Base Balance in
40. • Once Hemoglobin, becomes overwhelmed
Kidney excretes an increased chloride load
using NH4
+, a weak cation, for
electrochemical balance
• ―Metabolic compensation‖
Acid base regulation in respiratory
failure contd
41. • Metabolic acid is buffered principally by
increased alveolar ventilation ,
bicarbonate(imp), plasma proteins &
phosphate
• coupling of bicarbonate and H2O produces CO2
that is excreted through the lungs via an
increase in alveolar ventilation
• Chloride is preferentially excreted by the
kidney
Acid base regulation in metabolic
disorder
42. Compensation
A patient can be uncompensated, partially
compensated, or fully compensated
When an acid-base disorder is either
uncompensated or partially compensated, the
pH remains outside the normal range
In fully compensated states, the pH has
returned to near normal range
Body never overcompensates
43. Correct Terminology for
Compensatory Responses
According to the Ad-Hoc Committee , Secondary
or compensatory responses should NOT be
designated as acidosis or alkalosis.
Eg: A patient with diabetic ketoacidosis and
compensatory Kussmaul respirations should be
described as having a 'metabolic acidosis with
compensatory hyperventilation‘
The use of the term ‗secondary respiratory
alkalosis‘ in this case would be wrong
44. • Lactic acidosis is treated with volume
resuscitation and source control.
• Diabetic ketoacidosis is treated with volume
resuscitation and insulin.
• Renal acidosis is treated with dialysis
• Occasionally,treatment with intravenous
sodium bicarbonate is necessary
• (base excess × weight in kg)÷3
METABOLIC ACIDOSIS
TREATMENT AND CORRECTION
45. • A severe deficit (HCO3- < 10-12 mEq/L and pH<7.2)
should be corrected with sodium bicarbonate
• Useful if the acidosis is due to inorganic acids
• It is recommended that 50% of total deficit be given
over 3 to 4 hours. 7.5% NaHCO3
- contains 0.9 mEq/ml
• The usual initial target((desired HCO3- concentration):
10 - 12 mEq/L, which should bring the blood pH to
~7.20
• IV-push administration should be reserved for CPR
Ref:Koda-Kimble M, Young LY, et al. Handbook of Applied Therapeutics.
Lippincott Williams & Wilkins, 2006. P10.3(1104).
When and how to correct
46. • Key to managing acid-base disturbances lies
not in altering acid-base balance, but rather
in correcting the underlying defect
• Sodium bicarbonate is administered as an
7.5/8.4% hypertonic solution and has a
plasma-expanding effect that can lead to a
dilutional acidosis and increases PaCO2 as well
• Over-alkalinization causes decreased affinity
of hemoglobin for oxygen leading to tissue
hypoxia and lactic acid production ,Sodium
overload and hypokalemia.
Use of sodium bicarbonate boluses
or infusions is controversial
47. • Treat the primary cause.
• Potassium and magnesium should be
replaced.
• Dilute hydrochloric acid can be given orally
or intravenously.
• Acetazolamide can be considered.
METABOLIC ALKALOSIS
TREATMENT AND CORRECTION
48. • Increase alveolar ventilation.
• Associated hypophosphatemia should be
monitored.
RESPIRATORY ALKALOSIS
• Decrease in alveolar ventilation
• Hypoxaemia is an important cause of
respiratory alkalosis.
• Administration of oxygen in sufficient
concentrations and sufficient amount is
essential.
RESPIRATORY ACIDOSIS
TREATMENT AND CORRECTION
49. How to take an ABG Sample?
1. Site of puncture
2. Equipment required
3. Expel air bubbles
4. Keep sample in ice
5. Patient‘s inspired oxygen
concentration
50. • pH = 7.36 to 7.44
• PCO2 = 36 to 44 mmHg
• HCO3 = 22 to 26 mEq/L
• PaO2 = 80 to 100 mmHg
• SaO2 = 94 to 100 %
• Base excess = -2 to +2 mEq/L
NORMAL VALUES
51. • Stage I: Identify the Primary Acid-Base Disorder
• Rule 1: An acid-base abnormality is present if either
the PaCO2 or the pH is outside the normal range
• Rule 2: If both change in the same direction, the
primary acid-base disorder is metabolic, and if both
change in opposite directions, the primary acid-base
disorder is respiratory (ROME)
• Example: Consider a patient with an arterial pH of 7.23
and a PaCO2 of 23 mm Hg
• primary metabolic acidosis
A Stepwise Approach to Acid-Base
Interpretation
52. • Rule 3: If either the pH or PaCO2 is normal, there
is a mixed metabolic and respiratory acid-base
disorder (one is an acidosis and the other is an
alkalosis). If the pH is normal, the direction of
change in PaCO2 identifies the respiratory disorder,
and if the PaCO2 is normal, the direction of change
in the pH identifies the metabolic disorder
• Example: Consider a patient with an arterial pH of
7.4 and a PaCO2 of 55 mm Hg
• mixed respiratory acidosis and metabolic alkalosis
54. Disorder Acute Chronic
Resp. Acidosis pH decreases by 0.08
HCO3
- increases by 1
pH decreases by 0.03
HCO3
- increases by 4
Resp. Alkalosis pH increases by 0.08
HCO3
- decreases by 2
pH increases by 0.03
HCO3
- decreases by 5
Compensation for 10 mmHg change in PaCO2
in respiratory disturbances
55. • Rule 4: If there is a primary metabolic acidosis or
alkalosis, use the measured serum bicarbonate
concentration to identify the expected PaCO2
• Example: Consider a patient with a PaCO2 of 23
mm Hg, an arterial pH of 7.32, and serum HCO3 of
15 mEq/L.
• (1.5 × 15) + (8 ±2) = 30.5 ± 2 mm Hg.
primary metabolic acidosis with a superimposed
respiratory alkalosis
56. • Example: Consider a patient with a PaCO2 of 23
mm Hg and a pH of 7.54
7.40 + [0.008 × (40 - 23)] =7.54
acute respiratory alkalosis
If the measured pH was higher than 7.55
a superimposed metabolic alkalosis
Rule 5: If there is a respiratory acidosis or
alkalosis, use the PaCO2 to calculate expected pH
57. • The anion gap helps to classify met.acidosis
• The normal value is 12 ± 4 mEq/L
• High AG : lactic,ketoacidosis,ESRF,methanol
• Normal AG : diarrhea,saline infusion,RTA
• In hypoalbuminemia AG should be corrected
ANION GAP
Stage III: Use The “Gaps” to Evaluate Metabolic
Acidosis
58. • High AG metabolic acidosis, the gap-gap (AG
Excess/HCO3 deficit) ratio is unity (=1)
• Hyperchloremic acidosis, the ratio (AG
excess/∆HCO3 ) falls below unity (< 1)
• Therefore, in the presence of a high AG
metabolic acidosis, a ―gap-gap‖ (AG
excess/∆HCO3)ratio of less than 1 indicates
the co-existence of a normal AG metabolic
acidosis
• In the presence of a high AG metabolic
acidosis, a gap-gap (AG excess/∆HCO3 ) ratio
of greater than 1 indicates the co-existence of
a metabolic alkalosis.
The “Gap-Gap” ratio
59. • CASE 1: A 20 year old man is brought to the
emergency room with a history of consumption of
a bottle of pills.
• pH = 7.35
• PaCO2 = 15 mmHg
• HCO3
- = 8 mmolL-1
• Na+ = 140 mmolL-1
• K+ = 3.5 mmolL-1
• Cl - = 104 mmolL-1
• Step 1: Evaluate pH and narrow down to two
possible processes
• pH < 7.36 Acidosis (metabolic
or respiratory)
60. • Step 2: Evaluate the PaCO2 and narrow down to
one definitive process
PaCO2 < 40 mmHg ( metabolic
acidosis is present)
• Step 3: Apply the formula for metabolic acidosis
Predicted PaCO2 = 1.5 (HCO3
-) + 8
= 20mmHg
Actual PaCO2 = 15 mmHg
61. • Step 4: Determine if any other processes are
present
The actual PaCO2 is less than the predicted
Respiratory alkalosis
Diagnosis: Mixed metabolic acidosis +
Respiratory alkalosis
• Step 5: Evaluate anion gap
Anion gap = 140 - (104 + 8) = 28 (↑)
• Step 6: Evaluate gap-gap ratio
Delta gap= (28 - 12) / (24 - 8)= 16/16= 1
• Conclusion: Combined high anion gap
metabolic acidosis and Respiratory alkalosis
62. • A 44 year old moderately dehydrated man was
admitted with a two day history of acute severe
diarrhea. Electrolyte results: Na+ 134, K+ 2.9, Cl-
108, HCO3- 16, BUN 31, Cr 1.5.
• ABG: pH 7.31 pCO2 33 mmHg
HCO3 16 pO2 93 mmHg
• Based on the clinical scenario, likely acid base
disorders in this patient are:
• Normal anion gap acidosis from diarrhea or
• Elevated anion gap acidosis secondary to lactic
acidosis as a result of hypovolumia and poor
perfusion.
Case 2
63. • Look at the pH.
The pH is low, (less than 7.35) therefore by
definition, patient is acidemic.
• pH & pCO2 change in same direction(decrease)-
metabolic acidosis
• Is compensation adequate?
• Calculate the estimated PCO2.
Using Winter's formula; PCO2 = 1.5 × [HCO3-]+
8 ± 2 = 1.5 ×16 + 8 ± 2 = 30-34.
64. • Calculate the anion gap
The anion gap is Na - (Cl + HCO3-) = 134 -(108
+ 16) = 10
Since gap is less than 16, it is therefore normal
• Since the actual PCO2 falls within the estimated
range, we can deduce that the compensation is
adequate and there is no seperate respiratory
disorder present.
• Assessment: Normal anion gap acidosis with
adequate compensation most likely secondary to
severe diarrhea.
65. • 1) Is the "pH― normal?
• 2) Is the "CO2― normal?
• 3) Is the "HCO3― normal?
• 4) Apply ―ROME‖
• 5) Look for compensation
• 6) Are the "pO2― and the "O2― saturation normal?
The '6‗ Easy Steps to'ABG'Analysis
66. • pH normal, PCO2 increased
• Mixed disorder.
• Primary Respiratory acidosis
• Compensatory response?
• 7.4 – (0.003×20)
• [HCO3
-] to be increased by 4
• Respiratory acidosis with
metabolic alkalosis
67. • Conclusion
• The use of physical chemistry principles permits a
better explanation of acid-base balance and
provides tools to apply to a wide variety of clinical
situations. This does not suggest that the
―traditional‖ approach is incorrect. There is
currently no clear strategy to determine which of
the ‗modern‘ approaches, the Stewart approach or
the bicarbonate-centred approach , is the correct
one.
68. • Miller‘s anesthesia 7th edition
• The ICU book 3rd edition Paul L Marino
• A practice of Anesthesia 7th edition Wylie
• Lee‘s synopsis of Anaesthesia 13th edition
• Anaesthesia CME programme 2011 Mysuru
• A simple guide to blood gas analysis Peter
Driscoll
• www.acid-base.com
• www.acidbasedissorders.com
Bibliography