Arterial blood gas analysis assesment of oxygenation ventilation and acid base

ABG analysis of oxygenation/ ventilation /Acid base and indications of mechanical ventilation

1. Indications for Mechanical Ventilation
&

Dr. T.R.Chandrashekar
Chief -Department of Critical Care
K.R.Hospital, Bangalore
Karnataka, India
Arterial Blood Gas Analysis

2. Blood Gas Interpretation-means analyzing
the data to determine patient’s state of:
2
Ventilation
Oxygenation
Acid-Base
Discuss Indications for Mechanical Ventilation along with ABG interpretation
and clinical examples

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

4. Always mention and see…
FiO
2
/ ct Hb

-----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

5. 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

6. Matching delivery
=
Requirement
Assessment of Oxygenation
O2 delivery is a Cardio-Respiratory function

7. Oxygen Cascade
Atmospheric Air- 150 mmHg ( 21%)
PAO2-Alveolar Oxygen-100 mmHg ( CO2 / Water Vapour)
PaO2- 90mm Hg ( A-a difference)
SaO2 ( can be measured if Co-oximeter / calculated ODC)- Limitations

CaO2- Oxygen content (1.34 x Hb x Sao2)
DaO2-Oxygen delivery- CaO2 x Cardiac output
If A-a difference is
more -does it tell us
anything ?

8. OO
22
COCO
22
Alveoli
PAO2
Atmospheric air /FIO2
Water vapour is added-
Nose/ upper airway
Alveolar Oxygen
PaO
2 (2% dissolved O2)
Measured in ABG
P(A-a)O2
SaO2
O.
D.
C.
Temp
H+
2,3-DPG
98% of O2 is Hb bound-
1.34 x Hb% x Sao2
CaO2-oxygen content
+PaO2 x 0.003ml
Oxygen Delivery=CaO2 x Cardiac output
Cardiac output - SV x HR
Preload / Afterload/ Contractility
Oxygen delivery DO2 is a
Cardio- Respiratory Function
=

9. DO2-Oxygen delivery- CaO2 x Cardiac output
Did oxygen delivery meet
the demand?
Patient with sepsis on ventilator has
fever 103F ,BP 80/60 mmHg, HR 140/mt,
PaO2 100 mmHg, PcO2 42 mmHg, PH 7.23,
HCO3 20, SaO2 98%
Hb 12 gm%,
Not responding to Fluids/ inotropes
Delivery (DO2 )looks OK
How to assess the consumption?
Lactate-Anaerobic meatabolism
Lacti-time
ScVo2- oxygen saturation in Superior vena Cava
ScVO2
DO2
Consumption O2

10. CO2
O2
PaCO2=60 mmHg
PAO2 = FIO2 (BP-47) – 1.2 (PaCO2)
=.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 PaO2
FIO2
We always correlate PaO
2
with
FiO
2

BUT………………………….
never forget to correlate with
PaCO
2
PAO2=FIO2(Barometric Pressure-H2O)-1.2(PCO2)
PAO2 = FIO2 (760– 47 mm Hg)- 1.2 (PaCO2)
PAO2 = 0.21(713)-1.2(40)=100 mmHg
“1.2” is dropped when FIO2 is above 60%.
5 X FIO2=PaO2

11. 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
V/Q Mismatch-Dead Space
Shunt
P(A-a)O2 signifies some sort of
problem within the lungs

12. Oxygenation Physiology
PAO2
Diffusion defect
Pao2
Shunt
Does not respond to FIO2
Responds to FIO2
Diffusion defect is a rare cause
1µm
Oxygenation over within 1/3 time
If HR >240 it affects
CO2 has over 20 times more
Diffusion coefficient
Severe ARDS/ILD
CO2
Atmospheric air
Nitrogen

FIO2- O2
PaO2
V/Q Mismatch

13. Alveolar-arterial Difference
OO
22
COCO
22
Alveolar – arterial G.
100 - 45 = 55
……………… .Wide A-a
Oxygenation
Failure
Wide Gap
PCO
2
= 40
PaO
2
= 45
P
A
O
2
= 150 – 1.2 (40)
= 150 - 50
= 100
Ventilation
Failure
Normal Gap
PCO
2
= 80
PaO
2
= 45
PAO
2
=
150-1.2(80)
= 150-100
= 50

Alveolar arterial G.
50 – 45 = 5
…………… .Normal A-a

14. Interpretation of shunt fractions
<10%<10% NormalNormal
10-20%10-20% Mild shuntMild shunt
20-30%20-30% Significant shuntSignificant shunt
>30%>30% Critical shunt, even Critical shunt, even
100% O2 cannot 100% O2 cannot
restore Pao2restore Pao2

15. arterial-Alveolar O
2
tension ratio
a/A ratio
>0.75 normal
0.40-0.75 acceptable
0.29-0.39 poor
<0.20 very poor

16. a/A ratio
Nomogram

17. Oxygen Dissociation Curve: SaO2 vs. PaO2
CaO2
A B

18. Which patient is more hypoxemic, and why?
Patient A: pH 7.48, PaCO
2
34 mm Hg, PaO2 85 mm Hg,
SaO
2 95%, Hemoglobin 7 gm%-
Patient B: pH 7.32, PaCO
2
74 mm Hg, PaO2 59 mm Hg,
SaO
2
85%, Hemoglobin 15 gm%-
Patient A:
Arterial oxygen content = .95 x 7 x 1.34 = 8.9 ml O2/dl
Patient B:
Arterial oxygen content = .85 x 15 x 1.34 = 17.1 ml O2/dl
Hypoxic/Hypercarbic
Anemic
98% of O2 is Hb bound-
1.34 x Hb% x Sao2
+ ( 2% )PaO2 x 0.003mlCaO2 =

19. 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%

20. 20 vol%
15 vol %
O
2
Transport; Normal
= C.O X arterial O
2 content
5 L blood x150 /L blood x 1.39 ml O2/g Hb
(= 20 ml O
2
/dl blood, or 20 vol %
= 1000 ml O
2
/min
= 250 ml( oxygen consumption)
750 ml = Venous O
2
return( = 15 vol%)
DO
2

22. ScVO2-60%-80% normal range
Is the central venous oxygen saturation
measured from a CVP cannula
Reflects the global balance between oxygen
Delivery and consumption
ScVO2
SVO2
ScVO2 Range
60-80% Normal
60-50% More extraction
warning sign
50-30% Lactic acidosis
Demand > Supply
30-20% Severe lactic acidosis
Cell death
> 5-7

23. Factors which alter ScVo2
Decreased Delivery
DO2
Increased Consumption
VO2
Fever,
Shivering
Trauma
Pain / anxiety
Dysarhythmia
CCF/ MI
Sepsis
Hypoxia/hypoxemia
Suctioning,
ARDS/ COPD
Hemorrhage
Occult bleeding
RBC disorders
Anemia

24. 65 yr old male with DM IHD –in septic
shock on ventilator
ABG-PaO2-90 PH 7.42, PCO2 43
Hb-12 gm%, Spo2 98%
CaCo2-17 Vol%
BP 90/40 mmHg ,Temp 103F
What is the problem ?
ScVO2 48%, Lactate 8 mMoles/L
Fluids
Nor adrenaline / Dobutamine
Fever control
Case ….
65 yr old male with DM IHD –in septic
shock on ventilator
ABG-PaO2-90 PH 7.42, PCO2 43
Hb-12 gm%, Spo2 98%
CaCo2-17 Vol%
BP 90/40 mmHg ,Temp 103F
What is the problem ?
ScVO2 68%, Lactate 2 mMoles/L
Microcirculatory Mitochondrial
Dysfunction (MMDS)
ScVo2

25. Lactate metabolism
Glucose
Pyruvate Lactate
Oxidative
phosphorylation
2 ATP
36 ATP
NAD+CO2+H2O
O
2
+ NADH
Glycolysis
ADP
Cell
Cytoplasm
Mitochondria
Oxygen

26. c
Energy Failure and Lacti-Time
Aerobic
metabolism
36 ATP
Lack of O2 delivery
Anaerobic metabolism
2 ATP + Lactic acid
The time before lactate becomes less than 2 is
important prognostic indicator-LACTI- TIME
Septic patient admitted to ICU BP 90/50, HR 150/mt
ScVO2-45%, Lactate 6 mmoles/L ,PH 7.16,
PaO2/PCO2- 68/39 mmHg
After 2hrs- fluid
resuscitation/
Noradrenaline
BP140/80 mmHg
ScVo2-65% Lactate
3 mmoles/L
After 2hrs- fluid
resuscitation/
Noradrenaline
BP 70/40 mmHg
ScVo2-45% Lactate
7mmoles/L
Microcirculatory
mitochondrial
dysfunction (MMDS)

27. Summary –Oxygenation assessment
CaO2 x CO =Delivery
ScVO2=consumption
Lactate=Delivery not meeting demand
Anaerobic metabolism- decreased ATP
production -cell death
Lacti-Time- prognostic indicator

28. Assessment of Ventilatory Status….

29. Oxygenation Acid-Base
HCO3
PAO2 = FIO2 (BP-47) – 1.2 (PCO2) pH ~ ------------
PaCO2
PaO2
» VCO2 x .863
» PaCO2 = --------------------
» VA
» VA=Minute ventilation-Dead space volume
» f(VT) – f(VD)
PaCO2 is key to the blood gas universe; without understanding
PaCO2 you can’t understand oxygenation or acid-base.
The ONLY clinical parameter in PaCO2 equation is RR
VCO2=CO2 production

30. Breathing pattern’s effect on PaCO2
Patient Vt f Ve Description
A (400)(20) = 8.0L/min (slow/deep)
B (200)(40) = 8.0L/min (fast/shallow)
Patient Vt-Vd f Va
A (400-150)(20) =5.0L/min (slow/deep)
B (200-150)(40) =2.0L/min (fast/shallow)
PaCO2 = alveolar ventilation
Not on Minute ventilation which is measured
Dead space quantification at bed side not possible

31. 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
PaCO2 abnormalities…
PCO2-65 mmHg with rate 7/mt in Drug overdosage
65/7-true hypoventilation
PCO2-65 mmHg with rate 37/mt in bilateral consolidation
65/37- Reduced alveolar ventilation/ dead space ventilation
PCO2-22 mmHg with rate of 37/mt in post operative patient
with pain and fever-Increased alveolar ventilation

32. Quantification of Dead space
VD
VVTT
=
25-40% NORMAL (2ml/Kg)
In MV pts till 55% is normal
More than 60% is abnormal
dead space

33. Quantification of Dead spaceQuantification of Dead space
VD/VT=(PaCO2-PETCO2)/PaCO2
Minute volume in liters Ҳ PaCO2(mmHg)
Body weight in kg
Normal index<5
More than 8 indicates an increase dead space
Limitation-need to measure minute volume accurately
Difficulties in sampling and accurate measurement limits the usefulness
Of dead space in clinical practice

34. Case Scenarios ….
20 year old male with OP poisoning with
fasciculation's, neck muscle weakness with RR
35/mt, increased WOB, SPO2 on 4l/mt on RBM
84%, pooling secretions, HR 150/mt on atropine
drip, BP 140/60
ABG
PH 7.37
Pao2-52
Pco2-32
Do we intubate this guy?
YES
Intubated minimal settings
ABG stabilised
Has Pulse oximeter/ ETCO2
Do we require to repeat ABG’sNO
If pt develops hypotension
On inotrope /not synchronising
Yes

35. Treat the Patient not the ABG
ABG-PCO2-60mmHg,
PO2-58mmHg
with HR-80/min, BP-
130/80mmHg, RR-14/
min,
 A 45 yr old patient
with chronic
neurological
weakness conscious,
comfortable
ABG-PCO2-60mmHg,
PO2-58mmHg
and with
HR-120/min,BP-100/70
mmHg,RR-40/min,
A 24yr old asthmatic
severe respiratory
distress, drowsy
Intubate

36. Case Scenario….
40 yr old diabetic male pt with urinary sepsis
Has BP 90/60 mmHg after fluid resuscitation,
high dose noradrenaline,has tready pulse, is
tachypenic 35/mt with increased WOB-is
restless. On 6L of O2 RBM
ABG
PH-7.38
PaCO
2
-36 mmHg
PCO
2-
100 mmHg
Sao
2
-98%, ScVo2-50%, Lactate 6 mmoles/L
Do we intubate this patient
Normal respiratory effort-5% CO
Nearly 20-30% CO
Rest respiratory muscle and so CO
is utilised by essential organs

37. 55 year old chronic smoker, Diabetic male
admitted with Lower limb cellulitis has Sepsis
and Rt mid and lower zone pneumonia on 6L of
O2 on RBM
HR 140/mt
BP 100/60 mmHg
RR- 35 with increased WOB
ABG
PH-7.28
PaCO
2
-56 mmHg
PCO
2
- 58 mmHg
FIO2 70%
Pao2-58 hypoxemic
Pco2-56/35- decreased
Alveolar ventilation
Intubation

38. IF the same guy is already on 5L/O2 / on noradrenaline
fluid resuscitation- we probably intubate
40 yr old male Diabetic in
ketosis with pylonephritis
Drowsy received in casualty-
BP 70/50 mmHg, RR 28/mt,
Fever-103F, HR 150/mt, WOB
normal
SC-1.6 WBC 20,000, LFT
normal
ABG done on room air
PH-7.28
PCO
2
-36 mmHg
PaO
2
- 58 mmHg
HCO3 18 mmoles/L
O2 4L RBM
Fluids 2l
Noradrenaline
Imipenem +cilastin 1g IV,
Paracetamol
BP 140/80, HR 100/mt,
UO 100ml/hr
ABG
PH-7.38
PaCO
2
-36 mmHg
PCO
2
- 78 mmHg
HCO3 20 mmoles/L
Mentation better

39. A 29-year-old
woman has
excessive bleeding
normal delivery has
Hb of 5 g%,
fluids-3L/mt given
Bp 100/60mmHg
HR 114/mt
PH-7.38
PaCO
2-33 mmHg
PCO
2 - 78 mmHg
HCO3 22 mmoles/L
Cao2- 7 vol %
ScVO2 55 %
Lactate 5 mMoles/L
What do we do?
Packed cells
FFP
Platelet
1:1:1 (FFP to PRBC
to platelets)

40. Causes of Respiratory failure
Respiratory Center in Brain
Neuromuscular Connections
Thoracic Bellows
Airways (upper & lower)
Lung parenchyma (alveoli)
Head injury
Drug overdose
Spinal cord
injury
Myopathies
Myasthenia
C
COPD
ARDS
Brain
Nerves
Bellows
Airways
Alveoli
It only requires one disrupted
“link” to cause respiratory failure !

41. Some points which help us to decide when to
ventilate patients?
Primary cause for Respiratory failure-time for the
disease to resolve
Hypoxemia on high FIO2
Increased PCO2
Increased WOB
Airway protection ?
+ABG values
Do not treat the ABG, treat the patient
If you’re not sure whether or not the patient needs a
ventilator, the patient needs a ventilator

42. Shibu lijack
Acid Base analysisAcid Base analysis

43. 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)

44. Acid-Base Physiology

45. CO
2
+ H
2
O H
2
CO
3
H
+
+ HCO
3
-
CO
2
H
+
HCO
3
-
Acid-Base physiology
Respiratory
Metabolic
Ventilation controls PCO2
Kidney losses H+ and reabsorbs bicarbonate (HCO3-)
Bicarbonate is the transport from of CO2 hence should
move in the same direction
PCO2-Respiratory acidosis
(Hypoventilation)
PCO2-Respiratory alkalosis
(Hyperventilation)
HCO3- Metabolic acidosis
HCO3- Metabolic Alkalosis

46. 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

47. 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
HCO3-= 40/10
CO2=60/10
24/40
36/60
24/40
18/30

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

COMPENSATORY
RESPONSE
Metabolic
acidosis
¯ PH¯ HCO
3
-
¯ pCO2
Metabolic
alkalosis
­ PH­ HCO
3
-
­ pCO2
Respiratory
acidosis
¯ PH­ pCO2 ­ HCO
3
-
Respiratory
alkalosis
­ PH¯ pCO2 ¯ HCO
3
-

49. pH HCO
3
CO
2
7.20 15 40
7.25 15 30
7.37 15 20
Un Compensated
Partially Compensated
Fully Compensated
(pH abnormal)
(pH in normal range)

50. Body’s physiologic response to Primary disorder
in order to bring pH towards NORMAL limit
Full compensation
Partial compensation
No compensation…. (uncompensated)
BUT never overshoots,
If a overshoot pH is there,
Take it granted it is a MIXED disorder
Normal functioning

51. RESPIRATORY disorders…
Expected HCO
3
for a Change in CO
2
......... 1 2 3 4
Acidosis…. (expected) HCO
3
= 0.1 x ∆ CO
2

Alkalosis…. (expected) HCO
3
= 0.2 x ∆ CO
2

Acidosis…. (expected) HCO
3
= 0.35 x ∆ CO
2

Alkaosis…. (expected) HCO
3
= 0.4 x ∆ CO
2
Acute respiratory
Chronic respiratory
HCO3
-
( KIDNEY)
pCO2 (LUNG)
pH=
what has changed ? CO2

52. Compensation
Metabolic Acidosis: Compensation
Winters’ formula
pCO2 = 1.5 x [HCO3-] + 8 ± 2
Metabolic Alkalosis: Compensation
pCO2 = 0.7x [HCO3-] + 20 ± 5

53. Na+
Unmeasured
cations
Unmeasured
anions
Cl-
HCO3-
‘Mind the gap’
cations = Anions
Anion gap =
metabolic
acidosis

54. Anion Gap
AG = [Na
+
] - [Cl
-
+HCO3
-
]
•Elevated anion gap represents
metabolic acidosis
•Normal value: 12 ± 4mmol/L
•Major unmeasured anions
–albumin
–phosphates
–sulfates
–organic anions

55. -- Clinical history
-- pH normal, abnormal PCO
2
and HCO
3
-- PCO
2
and HCO
3
moving opposite directions
-- Degree of compensation for primary - disorder is inappropriate

57. 2. Look at pH?
3. Look up HcO3-// PCo2
4. Match either pCO2ot the HCO3with pH
5. Fix the level of compensation.
6.If metabolic acidosis, calculate-Anion gap
7.Correlate clinically
1. Consider the clinical settings! Anticipate the disorder
7 steps to analyze ABG

58. First Step-Clinical History
COPD- Chronic
Respiratory Acidosis-Met alkalosis
Asthma-Acute
Respiratory Acidosis not well compensated
Cardiac arrest-Acute
 Metabolic/Respiratory acidosis
Septic shock-Acute
 Metabolic acidosis

59. The second step
 Look at the pH - Label it.
pH of 7.30, PaCO2 of 80 mm Hg, and HCO3-
of 27 mEq/L. Na+ 143, CL-104
ACIDOSIS

60. Look at -pCO2. Label it.
pH of 7.30, PaCO2 of 80 mm Hg, and HCO3-
of 27 mEq/L.
Increased
Normal pCO2 levels Normal pCO2 levels
are 35-45mmHg. are 35-45mmHg.
Below 35 is alkalotic, Below 35 is alkalotic,
above 45 is acidic.above 45 is acidic.
The third step

61. • look at the HCO3- Label it.
pH of 7.30, PaCO2 of 80 mm Hg, and HCO3- of 27 mEq/L
•INCREASED
A normal HCO3 level is 22-26 A normal HCO3 level is 22-26
mEq/L. If the HCO3 is below 22, mEq/L. If the HCO3 is below 22,
the patient is acidotic. If the the patient is acidotic. If the
HCO3 is above 26, the patient HCO3 is above 26, the patient
is alkaloticis alkalotic

62. Next match either the pCO2 or the
HCO3 with the pH to determine the
acid-base disorder.
• pH of 7.30, PaCO2 of 80 mm Hg, and
HCO3- of 27 mEq/L
• pH is on acidotic side & PCO2 is increased.

So it is respiratory acidosis
The Fourth Step

63. •Does either the CO2 or HCO3 go in the
opposite direction of the pH?
•pH of 7.30, PaCO2 of 80 mm Hg, and HCO3-
of 27 mEq/L
•To find the primary and what is
compensatory
•HCO3 is going in opposite direction of
pH. So it is metabolic compensation
Fifth Step

64. RESPIRATORY disorders…
Expected HCO
3
for a Change in CO
2
......... 1 2 3 4
Acidosis…. (expected) HCO
3
= 0.1 x ∆ CO
2

Alkalosis…. (expected) HCO
3
= 0.2 x ∆ CO
2

Acidosis…. (expected) HCO
3
= 0.35 x ∆ CO
2

Alkaosis…. (expected) HCO
3
= 0.4 x ∆ CO
2
Acute respiratory
Chronic respiratory
HCO3
-
( KIDNEY)
pCO2 (LUNG)
pH=
what has changed ? CO2

65. Is the compensation full or partial??
Do the calculations….
pH of 7.30, PaCO2 of 80 mm Hg, and HCO3- of 27
mEq/L
PCO2 is increased by =40
HCO3-=should be increased by 4
i.e. 24+4=28( for full compensation)

66. •Calculate the anion gap if it is more
there is Metabolic acidosis
AG = [Na+] - [Cl- +HCO3-AG = [Na+] - [Cl- +HCO3-]]
Sixth Step
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

67. Pathogenesis of Metabolic Acidosis
with AG
Fixed acid accumulation and low serum bicarbonate
Renal failure Renal,GI Lactic Salicylate
Ketones Methanol
Phosphate Ethylene glycol
HCl
AG = [Na
+
] - [Cl
-
+HCO3
-
]

68. Equivalent rise of AG and Fall of HCO3……
….Pure Anion Gap Metabolic Acidosis
Discrepancy…….. in rise & fall
+ Non AG M acidosis, + M Alkalosis

69. 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

70. Finally

71. RESPIRATORY disorders…
Expected HCO
3
for a Change in CO
2
......... 1 2 3 4
Acidosis…. (expected) HCO
3
= 0.1 x ∆ CO
2

Alkalosis…. (expected) HCO
3
= 0.2 x ∆ CO
2

Acidosis…. (expected) HCO
3
= 0.35 x ∆ CO
2

Alkaosis…. (expected) HCO
3
= 0.4 x ∆ CO
2
Acute respiratory
Chronic respiratory
HCO3
-
( KIDNEY)
pCO2 (LUNG)
pH=
what has changed ? CO2

72. Compensation
Metabolic Acidosis: Compensation
Winters’ formula
pCO2 = 1.5 x [HCO3-] + 8 ± 2
Metabolic Alkalosis: Compensation
pCO2 = 0.7x [HCO3-] + 20 ± 5

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

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

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

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

77. 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

78. 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

79. 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.

80. 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.

81. 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.

82. 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.

83. 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.

84. [email protected]
• I shall practice gentle mechanical ventilation and not try
to bring ABG to perfect normal.
• I shall treat the patient not the ABG report
• I shall always correlate ABG report clinically

85. PaO2
O2 CASCADE
AIR
ALVEOLAR
POST PULMONARY
ARTERIAL
Hb
-MICRO
CIRCULATION
MIXED
VENOUS