1. Blood Gas Analysis Carrie George, MD Pediatric Critical Care Medicine
Adapted from Dr. Lara Nelson

2. Blood Gas Analysis
Acid-base status
Oxygenation

3. Anatomy of a Blood Gas pH/pCO2/pO2/HCO3 Base: metabolic
Oxygenation: lungs/ECMO
Acid: lungs/ECMO
The sum total of the acid/base balance,
on a log scale (pH=-log[H+])

4. Blood Gas Norms pH pCO2 pO2 HCO3 BE Arterial 7.35-7.45 35-45 80-100
22-26
-2 to +2
Venous
43-50
~45

5. Blood Gas Analysis Determine if pH is acidotic or alkalotic
Determine cause:
Respiratory
Metabolic
Mixed
3. Check oxygenation

6. Acid-Base Regulation Three mechanisms to maintain pH Respiratory (CO2)
Buffer (in the blood: carbonic acid/bicarbonate, phosphate buffers, Hgb)
Renal (HCO3-)

7. Acid-Base Equation: the carbonic acid/bicarbonate
CO2 + H2O H2CO HCO3- + H+
Respiratory component Blood/renal component
Acid Base

8. Acid vs. Alkaline Blood pH
Arterial pH = 7.40
Venous pH = 7.35
Acidosis Neutral pH Alkalosis

9. Etiology
Respiratory
Metabolic
Mixed

10. Rule #1
Every change in CO2 of 10 mEq/L causes pH to change by 0.08 (or Δ1 = 0.007)
Increased CO2 causes a decreases in pH
Decreased CO2 causes an increase in pH

11. Respiratory Acidosis Hypercarbia from hypoventilation Findings:
pCO2 increased therefore… pH decreases
Example:
ABG : /50/ /25

12. Respiratory Alkalosis
Hypercarbia from hypoventilation
Findings:
pCO2 decreased… therefore pH increases
Example:
ABG – 7.45/32/ /25

13. Metabolic Changes
Remember normal HCO3- is 22-26

14. Rule #2 Every change in HCO3- of 10 mEq/L causes pH to change by 0.15
Increased HCO3- causes an increase in pH
Decreased HCO3- causes a decrease in pH

15. Metabolic Acidosis Gain of acid – e.g. lactic acidosis
Inability to excrete acid – e.g. renal tubular acidosis
Loss of base – e.g. diarrhea
Example:
ABG – 7.25/40/ /15

16. Metabolic Alkalosis
Loss of acid – e.g. vomiting (low Cl and kidney retains HCO3-)
Gain of base – e.g. contraction alkalosis (lasix)
Example:
ABG – 7.55/40/ /35

17. Mixed pH depends on the type, severity, and acuity of each disorder
Over-correction of the pH does not occur

18. Practical Application
Check pH
Check pCO2
Remember Rule #1
Every change in CO2 of 10 mEq/L causes pH to change by 0.08

19. Practical Application cont.
4. Does this fully explain the results?
5. If not, remember Rule #2
Every change in HCO3- of 10 mEq/L causes pH to change by 0.15

20. Example #1 ABG- 7.30/48/ /22 Acidotic or Alkalotic? pCO2 High or Low?
pH change = pCO2 change?
Combined respiratory and metabolic acidosis

21. Example #2 ABG- 7.42/50/ /32 Acidotic or Alkalotic? pCO2 High or Low?
pH change = pCO2 change?
Metabolic alkalosis with respiratory compensation

22. Oxygen Supply and Demand
Arterial oxygen depends on:
-Lungs ability to get O2 into the blood
-Ability of hemoglobin to hold enough O2

23. Bedside Questions of Oxygenation
Does supply of O2 equal demand?
Is O2 content optimal?
Is delivery of O2 optimal?

24. Mixed Venous Saturation
SvO2: What is it?
-In simple terms, it is the O2 saturation of the blood returning to the right side of the heart
- This reflects the amount of O2 left after the tissues remove what they need
SvO2 = O2 delivered to tissues – O2 consumption

25. Oxygen Delivery
O2 transport to the tissues equals arterial O2 content x cardiac output
-DO2 = CaO2 x CO
- Normal DO2 = 1000 ml/min

26. Arterial Oxygen Content
CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x )
Normal CaO2 = 14 +/- 1 ml/ dl
Example:
CaO2 = (1.34 x 10 x 95)+(78 x )
= 12.97
If Hgb is 12, CaO2 = 15.52
If PaO22 is 150, CaO2 = 13.20

27. Mixed Venous Oxygen Content
CvO2 = (1.34 x Hgb x SvO2) + (PvO2 x )
Normal CvO2 = 14 +/- 1 ml/dl

28. Oxygen Consumption VO2 = (CaO2 – CvO2) x CO  Fick equation
Normal VO2 = 131 +/- 2 ml/min

29. Mixed Venous Saturation
SvO2 = O2 delivered to tissues – O2 consumption
How do we know what it is?
- Calculate it
- Direct blood gas analysis, e.g. from a pulmonary catheter
- Oximetry

30. Normal Mixed Venous Saturation
Normal value
-68%-77%
-Change from arterial saturation of 20% to 30%
Values less than 50% are worrisome, or a change of 40%- 50%
Values less than 30% suggest anaerobic metabolism
The most useful application is to follow trends

31. Oxygen Saturation and pO2
An O2 saturation of 75% correlates with a PaO2 of about 45 mmHg
This is on the step portion of the oxygen dissociation curve

32. Oxygen Dissociation Curve

33. Utility of MVO2
Gives information about the adequacy of oxygen delivery
Suggests information about oxygen consumption
Can help determine the usefulness of clinical interventions

34. Decreased MVO2
Oxygen delivery is not high enough to meet tissue needs.
Poor saturation
Anemia
Poor CO
Increased tissue extraction

35. Increased MVO2 Wedged PA catheter
Improvement in previous poor situation
Shunting
-Tissues no longer extracting oxygen
-How can you tell?

36. End-Organ Perfusion Brain - Neurologic exam Kidneys -Urine output
- Creatinine
Lacitic acidosis

37. NIRS Near Infrared Regional Spectroscopy
An alternative strategy for measuring localized perfusion

38. How the INVOS System Works
rSo2 index represents the balance of site-specific O2 delivery and consumption
It measures both venous (~75%) and arterial (~25%) blood
Indicates adequacy of site-specific tissue perfusion in real-time
Correlates positively with SvO2, but is site-specific and noninvasive
rSO2 is not a simple blood gas, it measures the amount of oxyhemoglobin in the tissue

39. Cerebral/Peri-Renal NIRS Monitoring

40. Cerebral rSO2 Normal values: - 30% less than the arterial saturation
- Even in cyanotic heart disease this is true
Concentrating values :
- A change of 20% from baseline
- rSO2 < 60%
As with MVO2 trends are the most helpful application

41. Peri-Renal rSO2 Normal Values:
- 10%-15% less than the arterial saturation
- Even in cyanotic heart disease this is true
Concerning values:
- A change of 20% from baseline
-rSO2 < 60%
As with MVO2 trends are the most helpful application

42. Why Monitor Both? More information is always better
Perfusion is differentially distributed, i.e. generally cerebral blood flow is maintained at the expense of other organs