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DEPARTMENT OF
ANESTHESIOLOGY
JJMMC, DAVANGERE.
SEMINAR ON ACID BASE BALANCE AND ABG ANALYSIS
CHAIR PERSON PRESENTED BY
Dr.RAVI.R Dr.GOPAN.G
PROFESSOR
DATE:14-6-2013
Over view
1. Basics concepts
2. History ;approaches
3. Acid base disorders &regulation
4. Treatment
5. interpretation
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
• 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
• 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
• 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
• Bicarbonate
• Haemoglobin
• Plasma proteins
• Phosphate
Minimise the change in pH
BUFFER
• 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
Carbon Dioxide–Bicarbonate
(Boston) Approach
• 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
• 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
Acid-base nomogram using the Copenhagen
approach (Crit Care Med26:1173-1179,1998)
• 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
Concept of anion gap
• 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
• Electric neutrality
• Dissociation equilibriums
• Mass conservation
Determined the hydrogen ion concentration of
ECF , by applying laws of :
Stewart Approach
• 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
―ANION GAP‖ Vs ―SIG‖
• The strong ion difference (SID)
• The total concentration of weak acids (ATOT).
• The PaCO2
Only three factors independently
affect acid-base balance
• ([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
• 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
Effect of changes in SID on hydrogen and hydroxyl ion
concentration. ( Can J Physiol Pharmacol 61:1444-
1461, 1983.)
• 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
• 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
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+]:
• [ 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
• Alterations in arterial carbon dioxide (PaCO2)
tension—respiratory acidosis or alkalosis
• Alterations in blood chemistry—metabolic
acidosis or alkalosis.
Acid-Base Abnormalities
Classification
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.
• 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
• 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
• Respiratory acidosis : narcosis, incomplete
reversal of neuromuscular blockade
• Respiratory alkalosis : anxiety
• Metabolic acidosis : Hypoperfusion,Hypotonic
fluid administration & Hyperchloremia
• Metabolic alkalosis : Massive blood
transfusion & nasogastric suctioning
Acid-Base Disturbances Commonly
Seen Perioperatively
• 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
• 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
• 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
• 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
• 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
• 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
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
• 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
• 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
• 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
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
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
• 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
• 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
• 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
• 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
• 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
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
• 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
• 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
• 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
• Metabolic acidosis
Expected PaCO2 = (1.5 × HCO3) + (8 ± 2)
• Metabolic Alkalosis
Expected PaCO2 = (0.7 × HCO3) + (21 ± 2)
Stage II: Evaluate Compensatory
Responses (winter’s formula)
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
• 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
• 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
• 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
• 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
• 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)
• 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
• 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
• 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
• 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.
• 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.
• 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
• 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
• 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.
• 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

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Acid base balance & ABG interpretation,Dept of anesthesiology,JJMMC,Davangere

  • 1. DEPARTMENT OF ANESTHESIOLOGY JJMMC, DAVANGERE. SEMINAR ON ACID BASE BALANCE AND ABG ANALYSIS CHAIR PERSON PRESENTED BY Dr.RAVI.R Dr.GOPAN.G PROFESSOR DATE:14-6-2013
  • 2. Over view 1. Basics concepts 2. History ;approaches 3. Acid base disorders &regulation 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
  • 7. • Bicarbonate • Haemoglobin • Plasma proteins • Phosphate Minimise the change in pH BUFFER
  • 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
  • 12. Acid-base nomogram using the Copenhagen approach (Crit Care Med26:1173-1179,1998)
  • 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
  • 18. ―ANION GAP‖ Vs ―SIG‖
  • 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
  • 31. • Respiratory acidosis : narcosis, incomplete reversal of neuromuscular blockade • Respiratory alkalosis : anxiety • Metabolic acidosis : Hypoperfusion,Hypotonic fluid administration & Hyperchloremia • Metabolic alkalosis : Massive blood transfusion & nasogastric suctioning Acid-Base Disturbances Commonly Seen Perioperatively
  • 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
  • 53. • Metabolic acidosis Expected PaCO2 = (1.5 × HCO3) + (8 ± 2) • Metabolic Alkalosis Expected PaCO2 = (0.7 × HCO3) + (21 ± 2) Stage II: Evaluate Compensatory Responses (winter’s formula)
  • 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