Arterial Blood Gas Analysis

2015

1. Dr. T.R.Chandrashekar
Intensivist, Liver transplantation.
BMC & RI super-specialty Hospital.
Bangalore.
Arterial Blood Gas Analysis

2. Why Order an ABG?
Aids in establishing a diagnosis
Helps guide treatment plan
Aids in ventilator management
Improvement in acid/base management allows
for optimal function of medications
Acid/base status may alter electrolyte levels
critical to patient status/care

3. Blood Gas Interpretation-means analyzing
the data to determine patient’s state of:
Ventilation
Oxygenation
Acid-Base

4. Approach to ABG Interpretation
Assessment
of Acid-Base
Status
Assessment of
Oxygenation &
Ventilation Status
There is an interrelationship, but less
confusing if considered separately…..
Volume –
Osmolality
Electrolytes

5. -----XXXX Diagnostics----
Blood Gas Report
Measured 37.0
0
C
pH 7.452
pCO2 45.1 mm Hg
pO2 112.3 mm Hg
Calculated Data
HCO3 act 31.2 mmol / L
O2 Sat 98.4 %
O2 ct 15.8
pO2 (A -a) 30.2 mm Hg 
pO2 (a/A) 0.78
Entered Data
FiO2 %
Ct Hb gm/dl

-----XXXX Diagnostics-----
Blood Gas Report
328 03:44 Feb 5 2006
Pt ID 3245 / 00
Measured 37.0
0
C
pH 7.452
pCO2 45.1 mm Hg
pO2 112.3 mm Hg
Corrected 38.6
0
C
pH 7.436
pCO2 47.6 mm Hg
pO2 122.4 mm Hg
Calculated Data
HCO3 act 31.2 mmol / L
HCO3 std 30.5 mmol / L
B E 6.6 mmol / L
O2 ct 15.8 mL / dl
O2 Sat 98.4 %
ct CO2 32.5 mmol / L
pO2 (A -a) 30.2 mm Hg 
pO2 (a/A) 0.78

Entered Data
Temp 38.6 0C
FiO2 30.0 %
ct Hb 10.5 gm/dl
Calculated parameters
Measured parameters
FIO
2
X 5=PaO
2

6. Why would I require a ABG ?
Oxygenation status?- Pulse oximeter SPO
2
✔
Ventilation status ? – ETCO
2
✔
Acid base status?
Stable patient
Normal hemodynamics
Good UO Surgical stress + Sick patient
Hepatic/ Renal dysfunction
Massive blood/ fluid usage
Specific surgeries- liver
transplantation/ Hypotensive
anaesthesia/ aortic surgeries
IHD/COPD/ Asthma ……

7. Assessment of Oxygenation
PaO
2
=Not informative
CaO
2
= DO
2
- Better
DO
2
~VO
2
=ScVO
2
and Lactate- Ideal
O
2
delivery is a Cardio-Respiratory function
TIME =TISSUE
Oxygen DonOxygen Don’t Go’t Go

Where the Blood Won’t FlowWhere the Blood Won’t Flow
Oxygen delivery DO
2
Oxygen requirement VO
2

8. Oxygen Cascade
Atmospheric Air- 150 mmHg ( 21%)
PAO
2
-Alveolar Oxygen-100 mmHg ( CO
2
/ Water Vapour)
PaO
2
- 90mm Hg ( A-a difference)
SaO
2
( can be measured if Co-oximeter / calculated ODC)- Limitations

CaO
2
- Oxygen content (1.34 x Hb x Sao2)
DaO
2
= Oxygen delivery = (CaO
2
x Cardiac output)
If A-a difference is
more -does it tell us
anything ?

9. OO
22
COCO
22
Alveoli
PAO
2
Atmospheric air /FIO
2
Water vapour is added-
Nose/ upper airway
Alveolar Oxygen
PaO
2 (2% dissolved O2)
Measured in ABG
SaO2
O.
D.
C.
98% of O2 is Hb bound-
1.34 x Hb% x Sao2
CaO
2
-oxygen content
+PaO
2
x 0.003ml
Oxygen Delivery=CaO
2 x Cardiac output
Cardiac output - SV x HR
Preload / Afterload/ Contractility
Oxygen delivery DO
2
is a
Cardio- Respiratory Function
=
Intra-operative bleeding Hb
Aspiration/ collapse
Cardiac depressants drugs/ MI
Stress response- Afterload
Causes for DO2

10. The power of hemoglobin
Normal Hypoxemia Anemia
PaO2 90 mm Hg45 mm Hg90 mm Hg
SaO2 98% 80% 98%
Hb 15 g/dL15 g/dL7.5 g/dL
CaO2 200 ml/L163 ml/L101 ml/L
% change - 18.6%- 49.5%
Restrictive transfusion strategy is the order of the day

11. PaCO2=60 mmHg
PAO
2
= FIO
2
(BP-47) – 1.2 (PaCO
2
)
=.21 (760- 47) – 1.2 (60)
= 150 – 72 = 78
An elevated PaCO
2
will lower the PAO
2
and as a result will lower the PaO
2
We always correlate PaO
2
with
FiO
2

BUT………………………….
never forget to correlate with
PaCO
2
PAO
2
=FIO
2
(Barometric Pressure-H
2
O)-1.2(PCO
2
)
PAO
2
= FIO
2
(760– 47 mm Hg)- 1.2 (PaCO
2
)
PAO
2
= 0.21(713)-1.2(40)=100 mmHg
“1.2” is dropped when FIO2 is above 60%.
PAO
2
is affected by PCO
2

12. A-aDo
2

A-aDo
2
= PAO
2
-PaO
2
(from ABG)= 10-15 mmHg / Increases with age

Increased P(A-a)O2 -lungs are not transferring oxygen properly from
alveoli into the pulmonary capillaries.

OO
2 2
COCO
22
PaO
2
Alveoli
PAO2
P(A-
a)O2
Diffusion defect
Interstitial edema ILD/ARDS
V/Q Mismatch-Dead Space
Amendable to increased FIO
2
Shunt ( >30%) not amendable to
increased FIO
2
/ May require PEEP
P(A-a)O2 signifies some sort of
problem within the lungs

13. If DO
2
is normal is everything OK?
Next question is
Is DO
2
~VO
2
?
Lactate levels
ScVO
2
/SVO
2
A central venous ABG may
be more informative than
arterial ABG
ScVO
2
DO
2
Consumption O
2

14. 75%
Factors that influence mixed and central venous Factors that influence mixed and central venous
SOSO
22
­VO2 ¯DO2 ­ DO2 ¯VO2
Stress
Pain
Hyperthermia
Shivering
¯ PaO2
¯ Hb
¯ Cardiac output
­ PaO2
­ Hb
­ Cardiac output
Hypothermia
Anesthesia
_
+
DO2 Oxygen delivery VO2 Oxygen requirement

15. Summary –Oxygenation assessment
CaO
2
x CO =Delivery
ScVO
2
& Lactate levels = Surrogates for DO
2
~VO
2
Lacti-Time- prognostic indicator
Is lactate bad? May not due to anaerobic metabolism
Body’s response to stress
Alternate energy shuttle
ScVO2 Range
60-80% Normal
60-50% More extraction
warning sign
50-30% Lactic acidosis
Demand > Supply
30-20% Severe lactic acidosis
Cell death
ScVO
2
SVO
2
> 5-7

16. 65 yr old male with DM IHD –in septic
shock on ventilator
ABG-PaO
2
-90 PH 7.42, PCO
2
43
Hb-12 gm%, Spo
2
98%
CaO
2
-17 Vol%
BP 90/40 mmHg ,Temp 103F
What is the problem ?
ScVO2 58%, Lactate 8 mMoles/L

Fluid resuscitation
Noradrenaline / Dobutamine
Fever control
After 2hrs
ScVO2 68%, Lactate 2 mMoles/L
Case …. PaO
2 and DO
2 are normal
65 yr old male with DM IHD –in septic
shock on ventilator
ABG-PaO
2
-90 PH 7.42,
PCO2
43
Hb-12 gm%, Spo2 98%
CaO
2
-17 Vol%
BP 70/40 mmHg ,Temp 102F
What is the problem ?
ScVO2 45% Lactate 10 mMoles/L
Microcirculatory Mitochondrial
Dysfunction (MMDS)

Fluid resuscitation
Noradrenaline / Dobutamine
Fever control
After 2hrs
ScVO2 38%, Lactate 14 mMoles/L
PaO
2
and DO
2
are normal

17. Assessment of Ventilatory Status….

18. Oxygenation Acid-Base
HCO
3
PAO
2
= FIO
2
(BP-47) – 1.2 (PCO
2
) pH ~ ------------
PaCO
2
PaO
2
» VCO
2
x .863
» PaCO
2
= --------------------
» VA
» VA=Minute ventilation-Dead space volume
» f(VT) – f(VD)
PaCO
2
is key to the blood gas universe; without understanding
PaCO
2
you can’t understand oxygenation or acid-base.
The ONLY clinical parameter in PaCO
2
equation is RR
VCO
2
=CO
2
production
Difficulties in sampling and accurate measurement limits the usefulness
Of dead space in clinical practice =2ml/kg

19. Breathing pattern’s effect on PaCO
2
Patient Vt f MV Description
A (400)(20) = 8.0L/min (slow/deep)
B (200)(40) = 8.0L/min (fast/shallow)
Patient Vt-Vd f Alveolar ventilation
A (400-150) (20) = 5.0L/min
B (200-150) (40) = 2.0L/min
PaCO
2
= alveolar ventilation
Not on Minute ventilation which is measured

20. Condition State of
PaCO2 in blood alveolar ventilation
> 45 mm Hg Hypercapnia Hypoventilation
35 - 45 mm Hg Eucapnia Normal ventilation
< 35 mm Hg Hypocapnia Hyperventilation
PaCO
2
abnormalities…
PCO
2
/ RR- 65 / 7 in Drug overdosage
True hypoventilation
PCO
2
/ RR - 65 / 37 in bilateral consolidation
Reduced alveolar ventilation/ dead space ventilation
PCO
2
/ RR - 22 / 37 in post operative patient with pain and fever-
Increased alveolar ventilation

21. Acid-Base DisturbancesAcid-Base Disturbances

22. Perioperative acid base disturbances
Sick patients +
Stress of surgery
Decreased organ perfusion
Reduced immunity
Activity of coagulation factors and
complement system impaired
Cardiac depression
Vasoplegia
Arrhythmias
Inotropes or vasopressors do not work
Reduced O
2
delivery
O
2
delivery is a Cardio-Respiratory function
Hypo perfusion— Anaerobic metabolism-Lactic acidosis
- More Cardiac depression and vasoplegia-Viscous cycle

23. There is always a underlying cause- treatment of which is
the most important step in acid base problems
Deodorant
Flush
Problem
.Patient has
Peritonitis/ Sepsis
BP 80/60 mmHg
pH of 7.12, HCO
3

14, Lactate of 6
PCO
2
23
Metabolic acidosis
NAHCO
3
Infusion to
correct pH
Fluid
resuscitation
Inotropes/
vasopressors
Surviving
Sepsis bundle

24. •Fever , pain, shivering-Increased metabolic demands
Limited cardio pulmonary reserves -more problems
•Narcotics , Sedatives, NMB –hypoventilation
•Nasogastric suctioning-Chloride loss- Metabolic alkalosis
•Hypotension may lead to lactic acidosis, renal dysfunction
Septic patients / Elderly / diabetic HT Nephropathy / IHD
Commonly encountered acid base
disturbances seen in Perioperative period

25. Basics
•[H+]= 40 nEq/L at pH-7.4
•For every 0.3 pH change = [H+] double
160nEq/L
40 nEq/L
16nEq/L
[ H
+
] in nEq/L = 10
(9-pH)

26. CO
2
+ H
2
O H
2
CO
3
H
+
+ HCO
3
-
CO
2
H
+
HCO
3
-
Acid-Base physiology
Respiratory
Metabolic
Bicarbonate is the transport from of CO
2
hence both should
move in the same direction
Ventilation controls PCO
2
Kidney losses H+ and reabsorbs bicarbonate (HCO
3
-
)
PCO
2
-Respiratory acidosis
(Hypoventilation)
PCO
2
-Respiratory alkalosis
(Hyperventilation)
HCO
3
-
- Metabolic acidosis
HCO
3
-
- Metabolic Alkalosis

27. Very fast 80% in ECF
Starts within minutes
good response by 2hrs,
complete by 12-24 hrs
Starts after few hrs
complete by 5-7 days

28. Acid-base Balance
Henderson-Hasselbalch Equation
[HCO3
-
]

pH = pK + log -------------
.03 [PaCO2]
For teaching purposes, the H-H equation can be
shortened to its basic relationships:
HCO3
-
( KIDNEY)
pH ~ --------------------

PaCO2 (LUNG)
Maximum compensation
HCO
3
-= 40/10
CO
2
=60/10

29. Stewart approach
•Stewart (physical chemistry principles) suggested that the
traditional Henderson-Hasselbalch explanation of the
underlying physiology and pathophysiology is wrong.
•“Traditional” approach merely looks at a mirror image of that
proposed by Stewart. In fact HH equation is a component of
Stewart approach
•The ‘‘modern’’ approach is clinically difficult, more CPU based
•Requires knowledge of protein and phosphate concentrations
and more electrolytes than may be routinely measured

30. Characteristics of 1° acid-base disorders
DISORDER PRIMARY
RESPONSES

COMPENSATORY
RESPONSE
Metabolic
acidosis
¯ PH¯ HCO
3
-
¯ pCO
2
Metabolic
alkalosis
­ PH­ HCO
3
-
­ pCO
2
Respiratory
acidosis
¯ PH­ pCO
2
­ HCO
3
-
Respiratory
alkalosis
­ PH¯ pCO
2
¯ HCO
3
-

31. pH HCO
3
CO
2
7.20 15 40
7.25 15 30
7.38 15 20
Un Compensated
Partially Compensated
Fully Compensated
(pH abnormal)
(pH in normal range)
This amount of compensation rarely occurs in Acute situations
Metabolic acidosis with compensatory Respiratory alkalosis

32. Body’s physiologic response to Primary disorder
in order to bring pH towards NORMAL limit
Full/Partial compensation/uncompensated
BUT never overshoots,
If overshoot pH is present -Take it for granted it is
a MIXED disorder
Normal functioning

33. •Clinical history
•pH normal, abnormal PCO
2
and HCO
3
•PCO
2
and HCO
3
moving in opposite directions
•Degree of anticipated compensation for primary disorder is
inappropriate??

34. Primary Respiratory disorders
Metabolic compensations

35. RESPIRATORY disorders CO
2
Change lead to change in HCO
3
Acidosis-expected change in HCO
3
= 1

Alkalosis-expected change in HCO
3
= 2 x

Acidosis-expected change in HCO
3
=3 x

Alkalosis-expected change in HCO
3
= 4 x
Acute respiratory
Chronic respiratory
For every 10 mmHg CO
2
change Expected HCO
3
Change is given below
Step 5 continued…CompensationStep 5 continued…Compensation

36. Primary Metabolic disorders
Respiratory compensations

37. Metabolic disorders compensation
by changing CO
2
Metabolic Acidosis: Compensation CO
2
Winters’ formula
pCO
2
= 1.5 x [HCO3-] + 8 ± 2
Last two digits of pH = PaCO
2
pH being 7.23 = PaCO
2
should fall to 23mmHg
Metabolic Alkalosis: Compensation CO
2
pCO
2
= 0.7x [HCO3-] + 20 ± 5
Unpredictable because increasing CO
2
causes increased RR

38. More anions are unmeasured than are
cations
Major unmeasured anions
•albumin
•phosphates
•sulfates
•organic anions- ketones and
lactate
Anion gap-AG = [Na
+
] - [Cl
-
+HCO
3
-
]
Anion gap is thus an artifact of
measurement, and not a physiologic reality
1 gm/dl decrease in serum albumin causes a 2.5 drop in the AG.
•Elevated anion gap represents metabolic acidosis
•Normal value: 12 ± 4mmol/L (More than 20 is usually significant)

39. [email protected]
•Practice gentle mechanical ventilation
and do not try to bring ABG to perfect
normal.
•Treat the patient not the ABG report

41. 2. Look at pH? (Acidosis /Alkalosis)
3. HCO
3
-
// PCO
2
(respiratory or metabolic or mixed )
4. Match either pCO
2
at the HCO
3
with pH
(which is primary & which is compensation)
5. Fix the level of compensation.
6.If metabolic acidosis, calculate-Anion gap
7. Treat the Patient not the ABG
1. Consider the clinical settings! Anticipate the disorder
7 steps to analyze ABG

42. 1
st
Step-Clinical History
COPD- Chronic
Respiratory Acidosis-Compensatory Met alkalosis
Post O.P patient -residual NMB, drowsy
Respiratory Acidosis not well compensated
Cardiac arrest
 Metabolic/Respiratory acidosis
Septic shock
 Metabolic acidosis

43. 2
nd
step
Look at the pH - Label it.
70 yr old man operated for # neck femur under
GA/ extubated drowsy shallow breathing on 2l
of O
2
Spo2 88%
ABG shows
pH of 7.28- ACIDOSIS
PaCO2 of 80 mm Hg,
HCO3- of 25 mEq/L.
Na+ 143, CL-104

44. Label it. (Respiratory or metabolic)
pH of 7.28,
PaCO2 of 80 mm Hg-Respiratory acidosis
 HCO3- of 25 mEq/L- Alkalosis
Normal pCONormal pCO
22 levels are 35-45mmHg. levels are 35-45mmHg.
Below 35 is alkalosis, Below 35 is alkalosis,
Above 45 is acidosis.Above 45 is acidosis.
3
RD
step-Look at -pCO
2
/ HCO
3
which
has moved in acidotic direction

45. Next match either -pCO
2
or HCO
3
with the pH
pH of 7.28-Acidosis
PaCO
2
of 80 mm Hg-Respiratory acidosis
HCO
3
- of 25 mEq/L- Compensatory alkalosis
pH and PCO
2
have moved in same direction
So it is Primary respiratory acidosis

4
TH
Step- Find the primary problem and what
is compensatory
HCO3- of 25 mEq/L is going in opposite direction of pH.
Metabolic compensation
Is it full/partial/uncompensated ???
Another disorder- mixed disorder ????

46. RESPIRATORY disorders- CO
2
Change lead to change in HCO
3
Acidosis-expected change in HCO
3
= 1

Alkalosis-expected change in HCO
3
= 2 x

Acidosis-expected change in HCO
3
=3 x

Alkalosis-expected change in HCO
3
= 4 x
Acute respiratory
Chronic respiratory
For every 10 mmHg CO
2
change expected HCO
3
Change is given below
Step 5 continued…CompensationStep 5 continued…Compensation

47. 5
TH
fix compensation- full or partial??
Do the calculations….
pH of 7.28,
PaCO2 of 80 mm Hg, (80-40=40 mmHg increased)
HCO3- of 25 mEq/L
PCO2 is increased by =40 (for every 10 rise in CO
2
/HCO
3

should increase by 1)
HCO3=should be increased by 4
i.e. 24+4=28( for full compensation)
Respiratory acidosis with partially compensated
metabolic alkalosis

48. •Calculate the anion gap if it is more
there is Metabolic acidosis
AG = [Na+] - [Cl- +HCO3-AG = [Na+] - [Cl- +HCO3-]]
Sixth Step- AG in case of metabolic acidosis
pH of 7.30, PaCO2 of 80 mm Hg, and
HCO3- of 27 mEq/L. Na+ 143, CL-104
AG+143- (104+27)=140-131=12

49. 7
Th
Step
Treat the Patient not the ABG
PCO
2
-60mmHg,
PO
2
-54mmHg
RR-40/min,
55 yr old patient with
chronic neurological
weakness conscious,
comfortable

PCO
2
-60mmHg,
PO
2
-54mmHg
RR-40/min,
Spinal surgery post OP
extubated with residual NMB
effect and drowsy
Severe respiratory distress
Reversal
/vent support

50. [email protected]
• Practice gentle mechanical ventilation and do not try to
bring ABG to perfect normal.
• Treat the patient not the ABG report

51. Too much normal saline hyperchloremic acidosis
Can we explain why increased Cl
-
causes Acidosis??

52. Normal saline infusion leads to
hyperchloremic acidosis
Dilution
of HCO
3
-
CO
2
CO
2
increases
HCO
3
-
unchanged
pH falls
Metabolic
CO
2

production
pH falls
Water H
2
O
dissociates
and adds H
+
Explanation of acidosis by HH method
Explanation of acidosis by Stewart
In NS- Na/Cl is 150 mEq/L
In ECF -Na 145/ Cl 102

53. Two approaches used in Acid
base evaluation
HCO3
-
( KIDNEY) 20
PaCO2 (LUNG) 1
pH ~
Metabolic’ component of
acid-base physiology is
bicarbonate
Stewart approachTraditional approach
Henderson-Hasselbalch
Water is an important source of H +
Ionic Strength: weak and strong
Electrical Neutrality is maintained at
all times
Metabolic’ component of acid-base
physiology is Strong Ion Difference (SID)
SID=(Na
+
+K
+
+Ca
2+
+Mg
2+
)-(Cl
-
+Lactate)
is 40 to 42 mEq/L

54. Two commonly used approaches
pH rely on three independent
Factors
1.SID- Strong ion difference
2.(A
TOT
)- total concentration of weak
acids (albumin and phosphate)
3.PCO2
‘Metabolic’ component of acid-base
physiology is not dependent on
bicarbonate but instead, predominately
on SID
Henderson-Hasselbalch
Stewart approach
HCO3
-
( KIDNEY)
PaCO2 (LUNG)
pH --------- ------~

55. Modified Stewart approach
= ([Na+] – [Cl-]) – 38 (1)

= 0.25x [4.2–albumin] (2)
Thus true BE = BE – [1 + 2]
At bedside- it works well!
{where 38 is normal average difference in strong ions – Na and Cl}
NaCl effect
Albumin effect
Story, Belmo, Balasubramanyam
where 4.2 is normal serum albumin

56. Base excess
The base excess is a calculated value that quantifies metabolic
derangements.
It hypothetically ‘‘corrects’’ pH to 7.4 by ‘‘adjusting’’ measured
PaCO2 to 40 mmHg, allowing a comparison of the ‘‘corrected’’
HCO3
with the normal HCO3.(i.e.,24mEq/L)at pH 7.4.
A negative value means that HCO3 stores are depleted.
Base excess=HCO
3
+10(pH-7.4)-24

58. Uncompensated
Respiratory Acidosis
pH = 7.4
PaCO2 = 40
HCO3 = 24
Post op pt –drowsy

59. Uncompensated
Respiratory Alkalosis
pH = 7.4
PaCO2 = 40
HCO3 = 24
Pt on vent pressure
support has pain
Acute asthmatic

60. Normal A.B.G.
pH = 7.4
PaCO2 = 40
HCO3 = 24

61. Partially compensated
Metabolic Acidosis
pH = 7.4
PaCO2 = 40
HCO3 = 24
20 yr old male with Acute Gastroenteritis…..

62. Case
A 46-year-old man has been in the hospital for two
days with pneumonia. He was recovering but has
just become diaphoretic, dyspneic, and
hypotensive. He is breathing oxygen through a
nasal cannula at 3 l/min.
pH 7.41
PaCO2 20 mm Hg
HCO3- 12 mEq/L
CaO2 17.2 ml O2/dl
PaO2 80 mm Hg
SaO2 95%
Hb 13.3 gm%
How would you characterize his state of oxygenation,
ventilation, and acid-base balance?
Normal pH
Respiratory alkalosis and
Metabolic acidosis.
Winters formula
pCo2=1.5 x 12 +8=26

63. Case
Mrs. H is found pulseless and not breathing this
morning. After a couple minutes of CPR she
responds with a pulse and starts breathing on
her own. A blood gas is obtained:
pH----------- 6.89
pCO
2
-------70
pO2 ---------42
HCO3------- 13
SaO2-------- 50%
What is your interpretation?
What interventions would be appropriate for
Mrs. H?
Mrs. H has a severe metabolic and
respiratory acidosis with hypoxemia

64. Case …..
A 44 year old moderately dehydrated man was
admitted with a two day history of acute severe
diarrhea. Electrolyte results: BP 90/60 mmHg
Na+ 134, K+ 2.9, Cl- 108,
BUN 31, Cr 1.5.
ABG: pH 7.31
 PCO2 33 mmHg
HCO3 16
 PaO2 93 mmHg
What is the acid base disorder?
History
Acidosis from diarrhea or
lactic acidosis as a result of
hypovolemia and poor
perfusion.

65. Normal anion gap acidosis with adequate compensation
 Look at the pH- acidemic.
 What is the process? Look at the PCO2, HCO3- .
PCO2 and HCO3- are abnormal in the same direction,
therefore less likely a mixed acid base disorder.
Calculate the anion gap
The anion gap is Na - (Cl + HCO3-) = 134 -(108 + 16) = 10

Is compensation adequate? Calculate the estimated PCO2.
Winter's formula;
PCO2 = 1.5 × [HCO3-]) + 8 ± 2 = 1.5 ×16 + 8 ± 2 = 30-34.

66. Case....
A 50 year old insulin dependent diabetic woman
was brought to the ED by ambulance. She was
semi-comatose and had been ill for several days.
Current medication was digoxin and a thiazide
diuretic for CHF.
Lab results
Serum chemistry:
 Na 132, K 2.7, Cl 79, Glu 815,
Lactate 0.9 urine ketones 3+
ABG: pH 7.41 PCO2 32
 HCO3- 19 pO2 82
History:
Elevated anion gap acidosis secondary to DKA
Metabolic alkalosis in the setting of thiazide
diuretics use.

67. Case......
2. Look at the pH. - Note that the pH is normal which would suggest no
acid base disorder. But remember, pH may be normal in the presence of a
mixed acid base disorder.
3. What is the process? Look at the PCO2, HCO3- .
PCO2 is low indicating a possible respiratory alkalosis. The HCO3- is also
low indicating a possible metabolic acidosis. Because the pH is normal, we
are unable to distinguish the initial, primary change from the compensatory
response.
We suspect however that the patient has DKA, and therefore should have a
metabolic acidosis with an anion gap that should be elevated. We can
confirm this by calculating the anion gap.
4. Calculate the anion gap
The anion gap is Na - (Cl + HCO3-) = 132 -(79 + 19) = 34
Since gap is greater than 16, it is therefore abnormal and confirms the
presence of metabolic acidosis.
Why is the pH normal? If the patient has metabolic acidosis, we suspect a
low ph unless there is another process acting to counteract the acidosis, i.e
alkalosis.

68. Delta Gap 34-12=22 + 19=41 Met alk
Since the delta ratio is greater than 2, we can
deduce that there is a concurrent metabolic
alkalosis. This is likely due to to the use of
thiazide diuretic. Note that DKA is often
associated with vomiting, but in this case;vomiting
was not mentioned.
Another possibility is a pre-existent high HCO3-
level due to compensated chonic respiratory
acidosis. But we have no reason to suspect
chronic respiratory acidosis based on the history.
Assessment: Mixed elevated anion gap
metabolic acidosis and metabolic alkalosis likely
due to DKA and thiazide diuretics.

69. Anion gap issues
A 1 gm/dl decrease in serum albumin causes a 2.5
mEq/L drop in the AG.
One problem with the anion gap is deciding what value is
truly abnormal.
In the majority of patients with anion gap between 16 and
20 mEq/L, no specific anion gap acidosis can be
diagnosed.
Above 20 mEq/L the probability of a true anion gap
acidosis increases markedly (and is 100% if the AG is
above 29 mEq/L)
As a practical matter, you should consider an AG 20
mEq/L as reflecting an anion gap metabolic acidosis and
search for the cause should be instituted

70. Delta gap = HCO
3 + ∆ AG
Delta Gap = 24….Pure AG acidosis
 < 24 = non AG acidosis
 > 24 = metabolic alkalosis
∆ AG =Measured Anion gap-12
Delta Gap = 24 …… AG Met Acidosis
< 24 ….. Non AG Met acidosis
> 24 ….. Non AG Met acidosis + Meta. Alkalosis

71. CaO2 = (1.34 x Hb x SaO2) +dissolved
O2
DO2 = CO X CaO2
Cardiac output
Mitochondria in end organs
7 g %
ALI/ARDS
PE
Sepsis induced
myocardial depression
Drugs
Inotropes
Pericardial effusion
vv
MMDS-cannot extract O2
O
2
lactate
CO
2
vv
aa

72. DO
2
/VO
2
Patients have to be kept well above the Critical Point so that
Does not plateau- Consumption remains supply
dependent even with supraphysiological levels
VO2 is supply
dependent
VO2 is supply independent
Oxygenation to the tissue is not compromised
MMDS and O2 extraction failure
Shunting due to micro-emboli