Documents
Resources
Learning Center
Upload
Plans & pricing Sign in
Sign Out

ARTERIAL BLOOD GAS

VIEWS: 9 PAGES: 30

									ARTERIAL BLOOD
    GASES
     Dr.Balamugesh
                  ABG - Introduction
   Blood gas and pH analysis has more immediacy
    and potential impact on patient care than any other
    laboratory determination.(National committee for Laboratory
    Standards).
   Cornerstone in the diagnosis & management of
    clinical oxygenation and acid-base disturbances.
   Of all the concepts employed in the diagnosis and
    treatment of respiratory disorders, few are more
    important or less well understood than those of
    blood gas interpretation.
  Information from ABGs

OXYGENATION

VENTILATION & ACID BASE
1. OXYGENATION:-
                   FiO2
               (0.21 – 1.0)
             P/F ratio


             A-a gradient


           PaO2
    2. VENTILATION & ACID
             BASE


CO2 +H2O      H2CO3      H+ + HCO3-




               Tissues



Expired CO2               H+
            Normal Ranges
PaO2 >80mm Hg
  – In supine posture PaO2=109-(0.43 Х age)
  – PaO2=100mmHg in 10 year old child, PaO2
    falls approximately 5mmHG for every 10 years
    upto 90 years.
  – 5 mmHg higher in the sitting position that
    supine position
                   Normals
   pH 7.35-7.45
   pCO2 35-45
   HCO3 24+2

Blood samples must be drawn only when the patient
  is in steady state.
20 to 30 min waiting period is recommended before
  taking ABG after a change in oxygen therapy or
  ventilation in those with pulmonary disease.
Sampling errors -Air contamination
 Most important change: PaO2 tends to
  increase towards 158mm Hg,
 Less significant change: PaCO2 falls, pH
  rises
 All air bubbles should be expelled
  immediately
 All samples with visually apparent froth
  should be discarded.
     Venous sampling/admixture
 Mixed venous blood – pH 7.38, pCO2 48mmHg,
                           PaO2 40mmHg, SaO2 75%
 Flash of blood on entering artery, pulsations during
  syringe filling, auto-filling of syringe, correlate
  with pulse oximetry.
 Addition of one-tenth of venous blood to an
  arterial sample could produce 25% drop in
  measure PaO2. Blood              Volume (ml)  PaO2
                    Arterial    4.5         86
                    Venous      0.5         31
                    Mixed       5.0         56
    Anticoagulant effects

   0.05ml of heparin(1,000units/ml) is required to
    anticoagulate 1 ml of blood.
   Dead space of a standard 5ml syringe with 22G
    needle is 0.2ml; i.e. filling the syringe dead space
    with heparin provides sufficient volume to
    anticoagulate a 4ml blood sample.
   Heparin – weak acid equilibrated with room air
   Initially PaCO2 falls,
   In extreme dilution pH and bicarbonate falls
   PaO2 usually unchanged.
 Time delay - metabolism
    Samples should be analyzed within 20 min
     to avoid error.
Measurement       Direction          Magnitude/Hour
pH                        ↓          0.05
PCO2                      ↑          5
PaO2                      ↓          20
                                     150 (initial
                                     >250mmHg)

Placing the sample in iced water slows metabolism to
10%.
   Leukocyte Larceny – Rapid fall in PaO2 in
    blood samples with high leukocyte counts –
    due to metabolism by leukocytes.
         Approach to Hypoxia
    Six basic mechanisms of hypoxia
1.   Decrease in inspired PO2
2.   Hypoventilation
3.   Shunting
4.   V/Q mismatching
5.   Diffusion barrier – least common cause
6.   Increased tissue consumption – not
     significant if lungs are normal
     Alveolar-arterial oxygen
      gradient(A-a gradient)
 Driving force for oxygen to enter blood
 Indicator of the extent of parenchymal
  dysfunction in the lung
 PAO2=[FiO2 Х (PB-PH20)] – PaCO2/R
 PAO2=150-[1.25 Х PaCO2]
 Normal= <15mmHg in <30yr old
 Increases by ~3mmHg per decade
 PaCO2=60; PaO2=35; pH=7.36.
 Mechanism of Hypoxia?
   AO2=150 – 1.25 Х 60 = 75
   A-a gradient=75-35=40.

Ans: hypoventilation with another
 mechanism.
          P/F ratio (PaO2/FiO2)
   Easy to calculate index of pulmonary
    parenchymal dysfunction
   Does not consider PaCO2.
   Normal 400-500
   Moderate pulmonary dysfunction 200-400
   Substantial pulmo. Dysfunction <200.
   Helps to decide the safe limits of reduction of
    FiO2 during weaning from oxygen.
   E.g: PaO2-160 on FiO2 of 0.8. If we want
    PaO2 of 80 reduce FiO2 to 0.4.
 Steps in Acid-base classification
1.   pH classification
2.   PaCO2 classification
3.   Metabolic classification
4.   Compensation evaluation
5.   Complete acid-base classification
        Verification of internal
             consistency
   Henderson-Hasselbalch equation

   pH=6.1 + HCO3 / ( 0.031 Х PCO2)
          pH classification
 7.35-7.45 – Normal
 <7.35 – acidosis
 >7.45 - alkalosis
         PaCO2 assessment
 Normal 35-45
 Respiratory acidosis >45
 Respiratory alkalosis<35
            Metabolic assessment
                      BE                  HCO3

  Normal              0 ±2                24 ±2

  Met.acidosis        <-2                 <22

  Met.alkalosis       >+2                 >26


Anion gap: Plasma anions not measured by routine laboratory.
AG= (Na+K) – (Cl+HCO3). Normal = 12 + 4 mEq/L
         Respiratory Acidosis
   In Respiratory Failure
 CO2 retention
 Causes –   from cerebral cortex to the
  peripheral nerve innervating respiratory
  muscle; from large airway to pleura..
 Treatment – mechanical ventilation,
  cause.
       Respiratory Alkalosis

 As in Hyperventilation
 Results in Hypocarbia
 Causes- Anxiety, cerebral stimulation,
  sepsis, drugs, hypoxia.
 Treatment - Cause, rebreathing
          Metabolic Acidosis-
 Check too much Heparin ??
 Increased Anion gap – Sepsis, renal Failure,
  Ketoacidosis, Drugs and Poisons
 Normal Anion Gap – GI-loss, Renal tubular
  acidosis, Endocrine (steroid def, renin def) Drugs
  ( Spironolactone, Amiloride, Triamterene )
 Treatment – Cause, Bicarb to replace buffer.
        Metabolic Alkalosis
 Causes –
- Vomiting as in Gastric outlet obstruction;
  loss of HCl acid,
- Renal with increased steroids,
- K+ depletion as with loop diuretics,
- Iatrogenic as with bicarbonate therapy.
Treatment – correct perpetuating cause(s):
 volume depletion, potassium correction
    Compensation assessment
 Return of an abnormal pH towards normal
  by the component that was not primarily
  affected.
 Body does not over compensate for a
  primary acid-base disturbance. In other
  words, when the pH reaches the normal
  range, compensatory mechanisms are no
  longer triggered.
            Expected compensation
Disorder                 Initial change   Compensation

Met. Acidosis             ↓ in HCO3       1.2 mmHg ↓in PCO2
                                          for every 1 ↓ in
                                          HCO3
Met. Alkalosis            ↑ in HCO3       0.6 ↑ in PCO2 for
                                          every 1 ↑ in HCO3
Resp.acidosis – Acute     ↑ in PCO2       1 ↑ in HCO3 for every
                                          10 ↑ in PCO2
Resp.acidosis –                           3.3 ↑ in HCO3 for
Chronic                                   every 10 ↑in PCO2
Resp.alkalosis – Acute    ↓ in PCO2       2.2 ↓ in HCO3 for
                                          every 10 ↓ PCO2
Resp.alkalosis –                          4.4 ↓ in HCO3 for
Chronic                                   every 10 ↓ in PCO2.
pH    PaCO2   HCO3   Diagnosis

7.6   30      31     MAlk+RAlk


7.1   70      14     MAci+RAci


7.5   25      21     RespAlk


7.4   20      12     MAc+Ralk


7.5   47      36     MAlk
THANK YOU

								
To top