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Arterial Blood Gas
      Interpretation

             PRESENTER- Dr. Garima Aggarwal
                             Resident IInd Yr
                      Department of Medicine

5th August    MODERATOR- Dr. Vikas Kesarwani
2011
OBJECTIVES
ABG    Sampling

Interpretation
              of ABG
 Oxygenation status
 Acid Base status

Case   Scenarios
ABG – Procedure and Precautions
   Site- (Ideally) Radial Artery
                   Brachial Artery
                   Femoral Artery

   Ideally - Pre-heparinised ABG syringes
            - Syringe should be FLUSHED with 0.5ml
        of 1:1000 Heparin solution and emptied.
        DO NOT LEAVE EXCESSIVE HEPARIN IN THE
                              SYRINGE

HEPARIN             DILUTIONAL                   HCO3
                       EFFECT                     PCO2
    Only small 0.5ml Heparin for flushing and discard it
    Syringes must have > 50% blood. Use only 2ml or less
     syringe.
   Ensure No Air Bubbles. Syringe must be sealed immediately
    after withdrawing sample.
    ◦ Contact with AIR BUBBLES
    Air bubble = PO2 150 mm Hg , PCO2 0 mm Hg
    Air Bubble + Blood = PO2       PCO2

   ABG Syringe must be transported at the earliest to the
    laboratory for EARLY analysis via COLD CHAIN
 Patients  Body Temperature affects the values of
    PCO2 and HCO3.
    ABG Analyser is controlled for Normal Body
     temperatures
    Any change in body temp at the time of sampling
     leads to alteration in values detected by the
     electrodes

      Cell count    in PO2

 ABG     Sample should always be sent with relevant
    information regarding O2, FiO2 status and Temp .
ABG ELECTRODES
A. pH (Sanz Electrode)
 Measures H+ ion concentration of sample against a
 known pH in a reference electrode, hence potential
 difference. Calibration with solutions of known pH (6.384
 to 7.384)

B. P CO2 (Severinghaus Electrode)
 CO2 reacts with solution to produce H+
   higher C02- more H+  higher P CO2 measured

C. P 02 (Clark Electrode)
 02 diffuses across membrane producing an electrical
 current measured as P 02.
Interpretation of ABG
 OXYGENATION
 ACID BASE
O    Determination  of PaO2
X   PaO2 is dependant upon                   Age, FiO2, Patm
Y   As Age       the expected PaO2
G
E    • PaO2 = 109 - 0.4 (Age)

N   As FiO2        the expected PaO2

A    • Alveolar Gas Equation:
T      • PAO2= (PB-P h2o) x FiO2- pCO2/R
I   PAO2 = partial pressure of oxygen in alveolar gas, PB = barometric pressure
    (760mmHg), Ph2o = water vapor pressure (47 mm Hg), FiO2 = fraction of
O   inspired oxygen, PCO2 = partial pressure of CO2 in the ABG, R = respiratory
    quotient (0.8)
N
 Determination            of the PaO2 / FiO2 ratio
Inspired Air FiO2 = 21%
PiO2 = 150 mmHg




PalvO2 = 100 mmHg




                          CO2                      O2

PaO2 = 90 mmHg




                                        (along with other criteria)
PO2/ FiO2 ratio ( P:F Ratio )
 Gives understanding that the patients
  OXYGENATION with respect to OXYGEN delivered
  is more important than simply the PO2 value.


 Example,
             Patient 1    Patient 2
            On Room Air   On MV

   PO2          60           90

   FiO2      21% (0.21)   50% (0.50)

   P:F          285          180
   Ratio
A                         Acid Base Balance
       H+ ion concentration in the body is
C       precisely regulated
I      The body understands the importance of H+
D       and hence devised DEFENCES against any
        change in its concentration-
B
A
S
E
    BICARBONATE              RESPIRATORY           RENAL
    BUFFER SYSTEM            REGULATION            REGULATION
    Acts in few seconds      Acts in few minutes   Acts in hours to days
Regulation of Acid Base
 Bicarbonate   Buffer System

CO2 + H2O carbonic anhydrase H2CO3     H+ + HCO3-

In Acidosis - Acid = H+
   H+ + HCO3       H2CO3     CO2 + H2O

In Alkalosis - Alkali + Weak Acid = H2CO3
   CO2 + H20      H2CO3         HCO3- + H+
                    +
                 ALKALI
 Respiratory Regulation   of Acid Base
 Balance-


                   ALVEOLAR
  H+               VENTILATION       PaCO2




                    ALVEOLAR
  H+                VENTILATION      PaCO2
 Renal   Regulation of Acid Base Balance
Kidneys control the acid-base balance by excreting
 either an acidic or a basic urine,
This is achieved in the following ways-


Reabsorption                                      Secretion of H+
 of HCO3                                           ions in tubules
 in blood                                          and excretion
             PCO2                                 K+
             in ECF
                                                       Aldosterone
    H+ ion            •Proximal Convulated
                      Tubules (85%)
                      •Thick Ascending Limb of
ECF Volume            Loop of Henle (10%)
                                                        Angiotensin II
                      •Distal Convulated Tubule
                      •Collecting Tubules(5%)
   Another mechanism by which the kidney
    controls the acid base balance is by the
    Combination of excess H+ ions in urine with
    AMMONIA and other buffers- A mechanism
    for generating NEW Bicarbonate ions


                       GLUTAMINE



REABSORBE           2HCO3-    2NH4+        EXCRETED
D                                               +
                                           H+, Cl-


   In CKD, the dominant mechanism by which acid
    is eliminated by the Kidneys is excretion of NH4+
Assessment of ACID BASE Balance
            Definitions and Terminology

 ACIDOSIS   – presence of a process which tends to
    pH by virtue of gain of H + or loss of HCO3-
 ALKALOSIS – presence of a process which tends
  to pH by virtue of loss of H+ or gain of HCO3-

If these changes, change pH, suffix ‘emia’ is added
 ACIDEMIA – reduction in arterial pH (pH<7.35)
 ALKALEMIA – increase in arterial pH (pH>7.45)
 Simple Acid  Base Disorder/ Primary Acid Base
 disorder – a single primary process of acidosis or
 alkalosis due to an initial change in PCO2 and HCO3.

 Compensation   - The normal response of
 the respiratory system or kidneys to change in pH
 induced by a primary acid-base disorder
 The Compensatory responses to a primary Acid Base
 disturbance are never enough to correct the change in
 pH , they only act to reduce the severity.

 Mixed Acid  Base Disorder – Presence of more than
 one acid base disorder simultaneously .
Characteristics of Primary ACID BASE
                   Disorders
PRIMARY       PRIMARY RESPONSES COMPENSATORY
DISORDER      H+ ion pH    Primary RESPONSES
              Conc.        Defect
Metabolic                               PCO2
Acidosis         H+   pH   HCO3        Alveolar
                                    Hyperventilation
Metabolic                               PCO2
Alkalosis        H+   pH   HCO3       Alveolar
                                    Hypoventilation
Respiratory
Acidosis         H+   pH    PCO2        HCO3

Respiratory
Alkalosis        H+   pH    PCO2        HCO3
Compensation
Metabolic Disorders – Compensation in these disorders leads to
a change in PCO2


                  • PCO2 = (1.5 X [HCO3-])+8 + 2
 METABOLIC • PCO2 = [HCO3-] + 15
  ACIDOSIS • For every 1mmol/l in HCO3 the PCO2
                    falls by 1.25 mm Hg



                  • PCO2 = (0.7 X [HCO3-])+ 21 + 2
 METABOLIC        • PCO2 = [HCO3-] + 15
 ALKALOSIS        • For every 1mol/l in HCO3 the PCO2
                    by 0.75 mm Hg
In Respiratory Disorders
    PCO2              Kidney              HCO3 Reabsorption
  Compensation begins to appear in 6 – 12 hrs and is fully
  developed only after a few days.

1.ACUTE
Before the onset of compensation
Resp. acidosis – 1mmHg in PCO2 HCO3 by 0.1meq/l
Resp. alkalosis – 1mmHg in PCO2 HCO3 by 0.2 meq/l

2.CHRONIC (>24 hrs)
After compensation is fully developed
Resp. acidosis – 1mmHg in PCO2          HCO3 by 0.4meq/l
Resp. alkalosis – 1mmHg in PCO2          HCO3 by 0.4meq/l
Respiratory Disorders – Compensation in these disorders
leads to a change in HCO3.

                 • ACUTE pH=7.40–0.008( PCO2-40)
RESPIRATORY
  ACIDOSIS  • CHRONIC pH=7.40–0.003(PCO2-40)



                  • ACUTE pH=7.40+0.008(40-PCO2)
RESPIRATORY
 ALKALOSIS
                  • CHRONIC pH=7.40+0.003(40-PCO2)
STEP WISE APPROACH
             to
      Interpretation Of
        ABG reports

Six steps logical approach originally proposed by Narins and
Emmett (1980) and modified by Morganroth in 1991
Normal Values
ANALYTE        Normal Value   Units

   pH           7.35 - 7.45

  PCO2            35 - 45     mm Hg

  PO2            72 – 104     mm Hg`

 [HCO3]          22 – 30      meq/L

  SaO2            95-100        %

Anion Gap         12 + 4      meq/L

 ∆HCO3           +2 to -2     meq/L
STEP 0   • Is this ABG Authentic?

STEP 1   • ACIDEMIA or ALKALEMIA?
         • RESPIRATORY or METABOLIC?
STEP 2

STEP 3 • If Respiratory – ACUTE or CHRONIC?
STEP 4 • Is COMPENSATION adequate?

STEP 5   • If METABOLIC – ANION GAP?

         • If High gap Metabolic Acidosis–
STEP 6     GAP GAP?
Is this ABG authentic ?
   pH = - log [H+]
        Henderson-Hasselbalch equation
                    pH = 6.1 + log HCO3-
                                  0.03 x PCO2
The [HCO3-] mentioned on the ABG is actually calculated
using this equation from measured values of PCO2 nd pH
          • [H+] neq/l = 24 X (PCO2 / HCO3)




                      •   pH = -log [ H+]
     pHexpected = pHmeasured = ABG is authentic
   Reference table for pH v/s [H+]
          H+ ion            pH
           100              7.00
            79              7.10
            63              7.20
            50              7.30
            45              7.35
            40              7.40
            35              7.45
            32              7.50
            25              7.60


       [H+] neq/l = 24 X (PCO2 / HCO3)
STEP 1          ACIDEMIA OR ALKALEMIA?



   Look at pH
             <7.35 - acidemia
             >7.45 – alkalemia

     RULE – An acid base abnormality is present even if
      either the pH or PCO2 are Normal.
STEP 2    RESPIRATORY or METABOLIC?

IS PRIMARY DISTURBANCE RESPIRATORY OR
METABOLIC?


pH   PCO2 or       pH    PCO2           METABOLIC

pH   PCO2 or pH          PCO2           RESPIRATORY

  RULE- If either the pH or PCO2 is Normal, there is a
  mixed metabolic and respiratory acid base disorder.
RESPIRATORY-
STEP 3                    ACUTE/CHRONIC?

IF RESPIRATORY, IS IT ACUTE OR CHRONIC?
Acute respiratory disorder - ∆pH(e-acute) = 0.008x ∆Pco2
Chronic respiratory disorder - ∆pH(e-chronic)= 0.003x ∆pCO2


Compare, pHmeasured (pHm)        v/s pHexpected (pHe)


                               pH(m) =
  pH(m) = pH(e- acute)   between pH(e- acute) &   pH(m) = pH(e-chronic)
                             pH(e- chronic)

ACUTE RESPIRATORY            PARTIALLY                  CHRONIC
    DISORDER               COMPENSATED                RESPIRATORY
                                                       DISORDER
STEP 4    ADEQUATE COMPENSATION?


IS THE COMPENSATORY RESPONSE ADEQUATE OR NOT?

METABOLIC DISORDER           PCO2expected
PCO2measured ≠ PCO2expected    MIXED DISORDER


RESPIRATORY DISORDER           pHexpected acute-chronic

pHm ≠ pHe range   MIXED DISORDER
STEP 0   • Is this ABG Authentic?

STEP 1   • ACIDEMIA or ALKALEMIA?
         • RESPIRATORY or METABOLIC?
STEP 2

STEP 3 • If Respiratory – ACUTE or CHRONIC?
STEP 4 • Is COMPENSATION adequate?

STEP 5   • If METABOLIC – ANION GAP?

         • If High gap Metabolic Acidosis–
STEP 6     GAP GAP?
Electrochemical Balance in Blood


100%      UC
                   UA
 90%
 80%               HCO3
         Na                 Sulfate
 70%                        Phosphate
 60%                        Mg- OA
                    Cl
 50%                        K - Proteins
 40%                        Ca-HCO3
 30%                        Na- Cl
 20%
 10%
  0%
       CATIONS   ANIONS
Anion Gap
AG based on principle of electroneutrality:

 Total Serum Cations = Total Serum Anions
 M cations + U cations = M anions + U anions
 Na + (K + Ca + Mg)       = HCO3 + Cl + (PO4 + SO4
                                     + Protein + Organic Acids)
 Na + UC                 = HCO3 + Cl + UA
 But in Blood there is a relative abundance of Anions, hence
             Anions       > Cations
 Na – (HCO3 + Cl)        = UA – UC
 Na – (HCO3 + Cl)        = Anion Gap
METABOLIC ACIDOSIS-
  STEP 5
                          ANION GAP?

IN METABOLIC ACIDOSIS WHAT IS THE ANION GAP?
       ANION        GAP(AG) = Na – (HCO3 + Cl)
           Normal Value = 12 + 4 ( 7- 16 Meq/l)

Adjusted Anion Gap = Observed AG +2.5(4.5- S.Albumin)
50%    in S. Albumin    75% in Anion Gap !!!

                         High Anion Gap Metabolic Acidosis
Metabolic Acidosis
                         Normal Anion Gap Acidosis
High Anion Gap Metabolic
Acidosis
   M
        METHANOL

   U
        UREMIA -     ARF/CRF
   D
        DIABETIC KETOACIDOSIS & other KETOSIS
   P
        PARALDEHYDE, PROPYLENE GLYCOL

    I
        ISONIAZIDE, IRON

    L
        LACTIC ACIDOSIS
   E
        ETHANOL, ETHYLENE GLYCOL

   S
        SALICYLATE
STEP 6            CO EXISTANT METABOLIC
                     DISORDER – “Gap Gap”?

C/O HGAG METABOLIC ACIDOSIS,ANOTHER DISORDER?
 ∆ Anion Gap = Measured AG – Normal AG
                   Measured AG – 12

∆ HCO3 = Normal HCO3 – Measured HCO3
                24 – Measured HCO3
Ideally,      ∆Anion Gap = ∆HCO3
For each 1 meq/L increase in AG, HCO3 will fall by 1 meq/L

∆AG/ HCO3- = 1  Pure High AG Met Acidosis
 AG/ HCO3- > 1  Assoc Metabolic Alkalosis
 AG/ HCO3- < 1  Assoc N AG Met Acidosis
Clinical
  CASE
SCENARIOS
CASE 1
Mr.
 Shamshuddin, 62/M         22/7/11    7:30 am
 ,                           pH          7.20
Nagina
 k/c/o COPD                PCO2      92 mmHg
 Breathlessness, progre
  ssively                   PO2       76 mmHg
  increased, aggravated
  on exertion, 2 days      Actual    21.00 mmol/l
 Chronic smoker           HCO3
 O/E                       SO2          89
  RS- B/L expiratory
  rhonchi                   FiO2        37%
 STEP 1 – ACIDEMIA
 STEP 2 – pH    PCO2
           Respiratory
 STEP 3 – pH expected
    pH acute = 7.40 – 0.008(92-40)
                7.40 – 0.008(52)
                6.984
    pH chronic = 7.40 – 0.003(92-40)
                   7.244
    pH b/w 6.98 to 7.244


 Primary     Respiratory Acidosis,
    partially compensated
CASE 2                                31/7/11     11:30pm

Mr.Dharam Dutt, 63/M,                   pH         7.18
Bijnor                                PCO2         21.00
 k/c/o CRF(conservativeRx)            PO2          90
 Breathlessness
                                      Actual       7.80
 Decreased Urine Otpt. 2days         HCO3
 Vomiting 10-15
                                    Base Excess    -18.80
 O/E
                                       SO2          95
    No pedal edema, dehydration +
    RS – B/L A/E Normal                 Na         140.6
                                     Chloride       102
                                     T.Protein       6
                                     Albumin        2.4
 STEP 1 – ACIDEMIA
 STEP 2 – pH       PCO2
           METABOLIC
 STEP 4 – PCO2expected
   PCO2exp = (1.5 x HCO3)+8+2
             (1.5X7.80)+8+2
              19.7+2= 17.7 – 21.7
 STEP5 – ANION GAP
         = Na – (HCO3 +Cl)
        = 140.6-(7.80+102)
        = 30.8
   AG corrected for albumin = 30.8+5.25
    AG = 36.05
HIGH AG Met. Acidosis
STEP 6 – GAP GAP
        = (AG-12)/(24-HCO3)
        = 36.05-12/24-7.80
        = 24.05/16.2
        = 1.48
Gap/gap > 1 = add. Metabolic
 alkalosis

∆sis – Primary Metabolic
  Acidosis
High Anion Gap, compensated
Cause- CRF
     - Metabolic Alkalosis
Cause - ? Vomiting
References
1)   Harrison’s Principles of Internal Medicine, 17th edition,
     Chap 48 – Acidosis and Alkalosis
2)   Paul L.Marino – The ICU Book, 3rd Edition
3)   Guyton and Hall – Textbook of Medical Physiology, 11th
     edition
4)   Davenport – The ABC of Acid Base Chemistry, 6th edition
5)   Cohen and Kassirer – Acid Base
6)   Hansen JE, Clinics in Chest medicine10(2), 1989, 227-37
7)   Lippincott’s-Fluid Balance, NM Metheny
8)   World Wide Web

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ABG Interpretation

  • 1. Arterial Blood Gas Interpretation PRESENTER- Dr. Garima Aggarwal Resident IInd Yr Department of Medicine 5th August MODERATOR- Dr. Vikas Kesarwani 2011
  • 2. OBJECTIVES ABG Sampling Interpretation of ABG Oxygenation status Acid Base status Case Scenarios
  • 3. ABG – Procedure and Precautions  Site- (Ideally) Radial Artery Brachial Artery Femoral Artery  Ideally - Pre-heparinised ABG syringes - Syringe should be FLUSHED with 0.5ml of 1:1000 Heparin solution and emptied. DO NOT LEAVE EXCESSIVE HEPARIN IN THE SYRINGE HEPARIN DILUTIONAL HCO3 EFFECT PCO2 Only small 0.5ml Heparin for flushing and discard it Syringes must have > 50% blood. Use only 2ml or less syringe.
  • 4. Ensure No Air Bubbles. Syringe must be sealed immediately after withdrawing sample. ◦ Contact with AIR BUBBLES Air bubble = PO2 150 mm Hg , PCO2 0 mm Hg Air Bubble + Blood = PO2 PCO2  ABG Syringe must be transported at the earliest to the laboratory for EARLY analysis via COLD CHAIN
  • 5.  Patients Body Temperature affects the values of PCO2 and HCO3. ABG Analyser is controlled for Normal Body temperatures Any change in body temp at the time of sampling leads to alteration in values detected by the electrodes  Cell count in PO2  ABG Sample should always be sent with relevant information regarding O2, FiO2 status and Temp .
  • 6. ABG ELECTRODES A. pH (Sanz Electrode)  Measures H+ ion concentration of sample against a known pH in a reference electrode, hence potential difference. Calibration with solutions of known pH (6.384 to 7.384) B. P CO2 (Severinghaus Electrode)  CO2 reacts with solution to produce H+ higher C02- more H+  higher P CO2 measured C. P 02 (Clark Electrode)  02 diffuses across membrane producing an electrical current measured as P 02.
  • 7. Interpretation of ABG  OXYGENATION  ACID BASE
  • 8. O  Determination of PaO2 X PaO2 is dependant upon Age, FiO2, Patm Y As Age the expected PaO2 G E • PaO2 = 109 - 0.4 (Age) N As FiO2 the expected PaO2 A • Alveolar Gas Equation: T • PAO2= (PB-P h2o) x FiO2- pCO2/R I PAO2 = partial pressure of oxygen in alveolar gas, PB = barometric pressure (760mmHg), Ph2o = water vapor pressure (47 mm Hg), FiO2 = fraction of O inspired oxygen, PCO2 = partial pressure of CO2 in the ABG, R = respiratory quotient (0.8) N
  • 9.  Determination of the PaO2 / FiO2 ratio Inspired Air FiO2 = 21% PiO2 = 150 mmHg PalvO2 = 100 mmHg CO2 O2 PaO2 = 90 mmHg (along with other criteria)
  • 10. PO2/ FiO2 ratio ( P:F Ratio ) Gives understanding that the patients OXYGENATION with respect to OXYGEN delivered is more important than simply the PO2 value. Example, Patient 1 Patient 2 On Room Air On MV PO2 60 90 FiO2 21% (0.21) 50% (0.50) P:F 285 180 Ratio
  • 11. A Acid Base Balance  H+ ion concentration in the body is C precisely regulated I  The body understands the importance of H+ D and hence devised DEFENCES against any change in its concentration- B A S E BICARBONATE RESPIRATORY RENAL BUFFER SYSTEM REGULATION REGULATION Acts in few seconds Acts in few minutes Acts in hours to days
  • 12. Regulation of Acid Base  Bicarbonate Buffer System CO2 + H2O carbonic anhydrase H2CO3 H+ + HCO3- In Acidosis - Acid = H+ H+ + HCO3 H2CO3 CO2 + H2O In Alkalosis - Alkali + Weak Acid = H2CO3 CO2 + H20 H2CO3 HCO3- + H+ + ALKALI
  • 13.  Respiratory Regulation of Acid Base Balance- ALVEOLAR H+ VENTILATION PaCO2 ALVEOLAR H+ VENTILATION PaCO2
  • 14.  Renal Regulation of Acid Base Balance Kidneys control the acid-base balance by excreting either an acidic or a basic urine, This is achieved in the following ways- Reabsorption Secretion of H+ of HCO3 ions in tubules in blood and excretion PCO2 K+ in ECF Aldosterone H+ ion •Proximal Convulated Tubules (85%) •Thick Ascending Limb of ECF Volume Loop of Henle (10%) Angiotensin II •Distal Convulated Tubule •Collecting Tubules(5%)
  • 15. Another mechanism by which the kidney controls the acid base balance is by the Combination of excess H+ ions in urine with AMMONIA and other buffers- A mechanism for generating NEW Bicarbonate ions GLUTAMINE REABSORBE 2HCO3- 2NH4+ EXCRETED D + H+, Cl-  In CKD, the dominant mechanism by which acid is eliminated by the Kidneys is excretion of NH4+
  • 16. Assessment of ACID BASE Balance  Definitions and Terminology  ACIDOSIS – presence of a process which tends to pH by virtue of gain of H + or loss of HCO3-  ALKALOSIS – presence of a process which tends to pH by virtue of loss of H+ or gain of HCO3- If these changes, change pH, suffix ‘emia’ is added  ACIDEMIA – reduction in arterial pH (pH<7.35)  ALKALEMIA – increase in arterial pH (pH>7.45)
  • 17.  Simple Acid Base Disorder/ Primary Acid Base disorder – a single primary process of acidosis or alkalosis due to an initial change in PCO2 and HCO3.  Compensation - The normal response of the respiratory system or kidneys to change in pH induced by a primary acid-base disorder  The Compensatory responses to a primary Acid Base disturbance are never enough to correct the change in pH , they only act to reduce the severity.  Mixed Acid Base Disorder – Presence of more than one acid base disorder simultaneously .
  • 18. Characteristics of Primary ACID BASE Disorders PRIMARY PRIMARY RESPONSES COMPENSATORY DISORDER H+ ion pH Primary RESPONSES Conc. Defect Metabolic PCO2 Acidosis H+ pH HCO3 Alveolar Hyperventilation Metabolic PCO2 Alkalosis H+ pH HCO3 Alveolar Hypoventilation Respiratory Acidosis H+ pH PCO2 HCO3 Respiratory Alkalosis H+ pH PCO2 HCO3
  • 19. Compensation Metabolic Disorders – Compensation in these disorders leads to a change in PCO2 • PCO2 = (1.5 X [HCO3-])+8 + 2 METABOLIC • PCO2 = [HCO3-] + 15 ACIDOSIS • For every 1mmol/l in HCO3 the PCO2 falls by 1.25 mm Hg • PCO2 = (0.7 X [HCO3-])+ 21 + 2 METABOLIC • PCO2 = [HCO3-] + 15 ALKALOSIS • For every 1mol/l in HCO3 the PCO2 by 0.75 mm Hg
  • 20. In Respiratory Disorders PCO2 Kidney HCO3 Reabsorption Compensation begins to appear in 6 – 12 hrs and is fully developed only after a few days. 1.ACUTE Before the onset of compensation Resp. acidosis – 1mmHg in PCO2 HCO3 by 0.1meq/l Resp. alkalosis – 1mmHg in PCO2 HCO3 by 0.2 meq/l 2.CHRONIC (>24 hrs) After compensation is fully developed Resp. acidosis – 1mmHg in PCO2 HCO3 by 0.4meq/l Resp. alkalosis – 1mmHg in PCO2 HCO3 by 0.4meq/l
  • 21. Respiratory Disorders – Compensation in these disorders leads to a change in HCO3. • ACUTE pH=7.40–0.008( PCO2-40) RESPIRATORY ACIDOSIS • CHRONIC pH=7.40–0.003(PCO2-40) • ACUTE pH=7.40+0.008(40-PCO2) RESPIRATORY ALKALOSIS • CHRONIC pH=7.40+0.003(40-PCO2)
  • 22. STEP WISE APPROACH to Interpretation Of ABG reports Six steps logical approach originally proposed by Narins and Emmett (1980) and modified by Morganroth in 1991
  • 23. Normal Values ANALYTE Normal Value Units pH 7.35 - 7.45 PCO2 35 - 45 mm Hg PO2 72 – 104 mm Hg` [HCO3] 22 – 30 meq/L SaO2 95-100 % Anion Gap 12 + 4 meq/L ∆HCO3 +2 to -2 meq/L
  • 24. STEP 0 • Is this ABG Authentic? STEP 1 • ACIDEMIA or ALKALEMIA? • RESPIRATORY or METABOLIC? STEP 2 STEP 3 • If Respiratory – ACUTE or CHRONIC? STEP 4 • Is COMPENSATION adequate? STEP 5 • If METABOLIC – ANION GAP? • If High gap Metabolic Acidosis– STEP 6 GAP GAP?
  • 25. Is this ABG authentic ?  pH = - log [H+] Henderson-Hasselbalch equation pH = 6.1 + log HCO3- 0.03 x PCO2 The [HCO3-] mentioned on the ABG is actually calculated using this equation from measured values of PCO2 nd pH • [H+] neq/l = 24 X (PCO2 / HCO3) • pH = -log [ H+] pHexpected = pHmeasured = ABG is authentic
  • 26. Reference table for pH v/s [H+] H+ ion pH 100 7.00 79 7.10 63 7.20 50 7.30 45 7.35 40 7.40 35 7.45 32 7.50 25 7.60 [H+] neq/l = 24 X (PCO2 / HCO3)
  • 27. STEP 1 ACIDEMIA OR ALKALEMIA?  Look at pH <7.35 - acidemia >7.45 – alkalemia  RULE – An acid base abnormality is present even if either the pH or PCO2 are Normal.
  • 28. STEP 2 RESPIRATORY or METABOLIC? IS PRIMARY DISTURBANCE RESPIRATORY OR METABOLIC? pH PCO2 or pH PCO2 METABOLIC pH PCO2 or pH PCO2 RESPIRATORY RULE- If either the pH or PCO2 is Normal, there is a mixed metabolic and respiratory acid base disorder.
  • 29. RESPIRATORY- STEP 3 ACUTE/CHRONIC? IF RESPIRATORY, IS IT ACUTE OR CHRONIC? Acute respiratory disorder - ∆pH(e-acute) = 0.008x ∆Pco2 Chronic respiratory disorder - ∆pH(e-chronic)= 0.003x ∆pCO2 Compare, pHmeasured (pHm) v/s pHexpected (pHe) pH(m) = pH(m) = pH(e- acute) between pH(e- acute) & pH(m) = pH(e-chronic) pH(e- chronic) ACUTE RESPIRATORY PARTIALLY CHRONIC DISORDER COMPENSATED RESPIRATORY DISORDER
  • 30. STEP 4 ADEQUATE COMPENSATION? IS THE COMPENSATORY RESPONSE ADEQUATE OR NOT? METABOLIC DISORDER PCO2expected PCO2measured ≠ PCO2expected MIXED DISORDER RESPIRATORY DISORDER pHexpected acute-chronic pHm ≠ pHe range MIXED DISORDER
  • 31. STEP 0 • Is this ABG Authentic? STEP 1 • ACIDEMIA or ALKALEMIA? • RESPIRATORY or METABOLIC? STEP 2 STEP 3 • If Respiratory – ACUTE or CHRONIC? STEP 4 • Is COMPENSATION adequate? STEP 5 • If METABOLIC – ANION GAP? • If High gap Metabolic Acidosis– STEP 6 GAP GAP?
  • 32. Electrochemical Balance in Blood 100% UC UA 90% 80% HCO3 Na Sulfate 70% Phosphate 60% Mg- OA Cl 50% K - Proteins 40% Ca-HCO3 30% Na- Cl 20% 10% 0% CATIONS ANIONS
  • 33. Anion Gap AG based on principle of electroneutrality:  Total Serum Cations = Total Serum Anions  M cations + U cations = M anions + U anions  Na + (K + Ca + Mg) = HCO3 + Cl + (PO4 + SO4 + Protein + Organic Acids)  Na + UC = HCO3 + Cl + UA  But in Blood there is a relative abundance of Anions, hence Anions > Cations  Na – (HCO3 + Cl) = UA – UC  Na – (HCO3 + Cl) = Anion Gap
  • 34. METABOLIC ACIDOSIS- STEP 5 ANION GAP? IN METABOLIC ACIDOSIS WHAT IS THE ANION GAP? ANION GAP(AG) = Na – (HCO3 + Cl) Normal Value = 12 + 4 ( 7- 16 Meq/l) Adjusted Anion Gap = Observed AG +2.5(4.5- S.Albumin) 50% in S. Albumin 75% in Anion Gap !!! High Anion Gap Metabolic Acidosis Metabolic Acidosis Normal Anion Gap Acidosis
  • 35. High Anion Gap Metabolic Acidosis M METHANOL U UREMIA - ARF/CRF D DIABETIC KETOACIDOSIS & other KETOSIS P PARALDEHYDE, PROPYLENE GLYCOL I ISONIAZIDE, IRON L LACTIC ACIDOSIS E ETHANOL, ETHYLENE GLYCOL S SALICYLATE
  • 36. STEP 6 CO EXISTANT METABOLIC DISORDER – “Gap Gap”? C/O HGAG METABOLIC ACIDOSIS,ANOTHER DISORDER?  ∆ Anion Gap = Measured AG – Normal AG Measured AG – 12 ∆ HCO3 = Normal HCO3 – Measured HCO3 24 – Measured HCO3 Ideally, ∆Anion Gap = ∆HCO3 For each 1 meq/L increase in AG, HCO3 will fall by 1 meq/L ∆AG/ HCO3- = 1  Pure High AG Met Acidosis AG/ HCO3- > 1  Assoc Metabolic Alkalosis AG/ HCO3- < 1  Assoc N AG Met Acidosis
  • 38. CASE 1 Mr. Shamshuddin, 62/M 22/7/11 7:30 am , pH 7.20 Nagina  k/c/o COPD PCO2 92 mmHg  Breathlessness, progre ssively PO2 76 mmHg increased, aggravated on exertion, 2 days Actual 21.00 mmol/l  Chronic smoker HCO3  O/E SO2 89 RS- B/L expiratory rhonchi FiO2 37%
  • 39.  STEP 1 – ACIDEMIA  STEP 2 – pH PCO2 Respiratory  STEP 3 – pH expected pH acute = 7.40 – 0.008(92-40) 7.40 – 0.008(52) 6.984 pH chronic = 7.40 – 0.003(92-40) 7.244 pH b/w 6.98 to 7.244  Primary Respiratory Acidosis, partially compensated
  • 40. CASE 2 31/7/11 11:30pm Mr.Dharam Dutt, 63/M, pH 7.18 Bijnor PCO2 21.00  k/c/o CRF(conservativeRx) PO2 90  Breathlessness Actual 7.80  Decreased Urine Otpt. 2days HCO3  Vomiting 10-15 Base Excess -18.80  O/E SO2 95 No pedal edema, dehydration + RS – B/L A/E Normal Na 140.6 Chloride 102 T.Protein 6 Albumin 2.4
  • 41.  STEP 1 – ACIDEMIA  STEP 2 – pH PCO2 METABOLIC  STEP 4 – PCO2expected PCO2exp = (1.5 x HCO3)+8+2 (1.5X7.80)+8+2 19.7+2= 17.7 – 21.7  STEP5 – ANION GAP = Na – (HCO3 +Cl) = 140.6-(7.80+102) = 30.8  AG corrected for albumin = 30.8+5.25 AG = 36.05 HIGH AG Met. Acidosis
  • 42. STEP 6 – GAP GAP = (AG-12)/(24-HCO3) = 36.05-12/24-7.80 = 24.05/16.2 = 1.48 Gap/gap > 1 = add. Metabolic alkalosis ∆sis – Primary Metabolic Acidosis High Anion Gap, compensated Cause- CRF - Metabolic Alkalosis Cause - ? Vomiting
  • 43. References 1) Harrison’s Principles of Internal Medicine, 17th edition, Chap 48 – Acidosis and Alkalosis 2) Paul L.Marino – The ICU Book, 3rd Edition 3) Guyton and Hall – Textbook of Medical Physiology, 11th edition 4) Davenport – The ABC of Acid Base Chemistry, 6th edition 5) Cohen and Kassirer – Acid Base 6) Hansen JE, Clinics in Chest medicine10(2), 1989, 227-37 7) Lippincott’s-Fluid Balance, NM Metheny 8) World Wide Web