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Blood Gas Analysis
Carrie George, MDPediatric Critical Care MedicineAdapted from Dr. Lara Nelson
Blood Gas Analysis• Acid-base status • Oxygenation
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+])
Blood Gas Norms
pH pCO2 pO2 HCO3 BE
Arterial 7.35-7.45 35-45 80-100 22-26 -2 to +2
Venous 7.30-7.40 43-50 ~45 22-26 -2 to +2
Blood Gas Analysis
1. Determine if pH is acidotic or alkalotic
2. Determine cause:1. Respiratory2. Metabolic3. Mixed
3. Check oxygenation
Acid-Base Regulation
• Three mechanisms to maintain pH– Respiratory (CO2)– Buffer (in the blood: carbonic
acid/bicarbonate, phosphate buffers, Hgb)
– Renal (HCO3-)
Acid-Base Equation: the carbonic acid/bicarbonate
CO2 + H2O H2CO3 HCO3- + H+
Respiratory component Blood/renal component Acid Base
• Arterial pH = 7.40• Venous pH = 7.35
6.9 7.0 7.4 7.5
Acidosis Neutral pH Alkalosis
Acid vs. Alkaline Blood pH
Etiology
• Respiratory• Metabolic• Mixed
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
Respiratory Acidosis
• Hypercarbia from hypoventilation• Findings:
– pCO2 increased therefore… pH decreases
• Example:ABG : 7.32/50/ /25
Respiratory Alkalosis
• Hypercarbia from hypoventilation• Findings:
– pCO2 decreased… therefore pH increases
• Example:ABG – 7.45/32/ /25
Metabolic Changes
• Remember normal HCO3- is 22-26
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
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
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
Mixed
• pH depends on the type, severity, and acuity of each disorder
• Over-correction of the pH does not occur
Practical Application
1. Check pH2. Check pCO23. Remember Rule #1
Every change in CO2 of 10 mEq/L causes pH to change by 0.08
Practical Application cont.
4. Does this fully explain the results?
5. If not, remember Rule #2Every change in HCO3- of 10 mEq/L causes pH to change by 0.15
Example #1
• ABG- 7.30/48/ /22• Acidotic or Alkalotic?• pCO2 High or Low?• pH change = pCO2 change?
Combined respiratory and metabolic acidosis
Example #2
• ABG- 7.42/50/ /32• Acidotic or Alkalotic?• pCO2 High or Low?• pH change = pCO2 change?
Metabolic alkalosis with respiratory compensation
Oxygen Supply and Demand
Arterial oxygen depends on:-Lungs ability to get O2 into the blood-Ability of hemoglobin to hold enough O2
Bedside Questions of Oxygenation
• Does supply of O2 equal demand?• Is O2 content optimal?• Is delivery of O2 optimal?
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
Oxygen Delivery
O2 transport to the tissues equals arterial O2 content x cardiac output-DO2 = CaO2 x CO
- Normal DO2 = 1000 ml/min
Arterial Oxygen Content
• CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x 0.0031)
• Normal CaO2 = 14 +/- 1 ml/ dl• Example:
CaO2 = (1.34 x 10 x 95)+(78 x 0.0031)
= 12.97If Hgb is 12, CaO2 = 15.52
If PaO22 is 150, CaO2 = 13.20
Mixed Venous Oxygen Content
• CvO2 = (1.34 x Hgb x SvO2) + (PvO2 x 0.0031)
• Normal CvO2 = 14 +/- 1 ml/dl
Oxygen Consumption
• VO2 = (CaO2 – CvO2) x CO
Fick equation• Normal VO2 = 131 +/- 2 ml/min
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
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
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
Oxygen Dissociation Curve
Utility of MVO2
• Gives information about the adequacy of oxygen delivery
• Suggests information about oxygen consumption
• Can help determine the usefulness of clinical interventions
Decreased MVO2
Oxygen delivery is not high enough to meet tissue needs.
• Poor saturation• Anemia• Poor CO• Increased tissue extraction
Increased MVO2
• Wedged PA catheter• Improvement in previous poor
situation• Shunting
-Tissues no longer extracting oxygen-How can you tell?
End-Organ Perfusion
• Brain- Neurologic exam
• Kidneys-Urine output
- Creatinine• Lacitic acidosis
NIRS
• Near Infrared Regional Spectroscopy
• An alternative strategy for measuring localized perfusion
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
Cerebral/Peri-Renal NIRS Monitoring
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
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
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