The document discusses arterial blood gas analysis and interpretation. It provides two scenarios to consider for intubation decisions based on clinical presentation and ABG values. It then presents five cases and asks which would warrant immediate ventilatory support. Key points about ABG components, indications for airway/ventilation support, and the approach to ABG interpretation focusing on assessment of ventilation, oxygenation, and acid-base balance are summarized.

1. Arterial blood gas analysis
DR AYUSHMAN

2. Decision to intubate
• The decision to intubate should be primarily made on
clinical grounds and the figures in ABG values like
PaO2<60 mmHg, PCO2>55mmHg etc should be used as
a guideline only
Consider two scenarios:
• A 45 yr old patient with chronic neurological weakness
with PCO2-60mmHg, PO2-58mmHg and with HR-80/min,
BP- 130/80mmHg, RR-14/min, conscious, comfortable
• A 24yr old asthmatic with PCO2-60mmHg, PO2-58mmHg
and with HR-120/min,BP-100/70 mmHg,RR-40/min, in
severe respiratory distress, drowsy

3. Which of the following cases would warrant
immediate ventilatory support?
a. A 50-year-old man iscomatose from drug overdose.
PaCO2 is51 mm Hg, PaO2 is76 mm Hg, and pH is7.31
while breathing room air.
b. A 29-year-old man is restless and in severe respiratory
distress; he is breathing 42 times/min. PaCO2 is 33 mm
Hg. pH is 7.42, and PaO2 is 47 mm Hg while breathing
60% oxygen through a face mask.
c. A 61-year-old woman who has severe emphysema is
alert but isin moderate respiratory distress; her
respiratory rate is24/min. PaO2 is75 mm Hg while
breathing nasal oxygen at 2 L/min, PaCO2 is 59 mm Hg,
and the pH is7.34. Her chest x-rayisclear.

4. d. A 29-year-old woman issuffering from diabetic
ketoacidosis. Her pH is7.15, PaCO2 is26 mm Hg and
PaO2 is 110 mm Hg while breathing room air.
e. A 31-year-old drug addict responds briefly to the
administration of Narcan (a narcotic antagonist) by
opening her eyes and crying out and then lapses back
into a state of semi-stupor. PaCO2 is31 mm Hg. pH is
7.38, and PaO2 is90 mm Hg while breathing nasal
oxygen at 3L/min.

5. Indications for Definitive
Airway/Ventilatory support
Need for Airway Protection
Unconscious
Severe Maxillofacial Injuries
Riskfor aspiration
• Bleeding
• Vomiting
Riskfor obstruction
• Neck hematoma
• Laryngeal, tracheal injury/burn
• Stridor
Need for Ventilation
Apnea
• Neuromuscular Paralysis
• Unconscious
Inadequate Respiratory Effort
• Tachypnea
• Hypoxia
• Hypercarbia
• Cyanosis
Severe head injury with need for
controlling PaCO2 level
• Any patient in cardiac arrest
• Haemodynamic instability due
to septic or cardiogenic shock

6. What isan ABG?
• The Components
– pH / PaCO2 / PaO2/ HCO3 / O2sat / BE
• Desired Ranges
–pH : 7.35 -7.45
– PaCO2 : 35-45 mmHg
–PaO2 : 80-100 mmHg
–HCO3 : 22-26mEq/L
–O2sat : 93-100%
– Base Excess : +/-2 mEq/L

7. 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

8. Approach to ABGInterpretation
Assessment
of Acid-Base
Status
Assessmentof
Oxygenation &
ventilatory
Status
There isan interrelationship, but less
confusing if considered separately…..

9. The Key to Blood Gas Interpretation:
Four Equations, Three Physiologic Processes
Equation Physiologic Process
Alveolar ventilation
Oxygenation
Oxygenation
Acid-base balance
1. PaCO2equation
2. Alveolar gas equation
3. Oxygen content equation
4. Henderson-Hasselbalch
equation

10. Assessment of Ventilatory Status….

11. 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 level isdependent on alveolarventilation

12. 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…

13. • Assessment of Oxygenation….

14. ASSESSMENTOFOXYGENATION
• How much oxygen is in the blood?
PaO2 vs. SaO2 vs. CaO2
• Alveolar-arterial O2 tension difference
• PaO2/FIO2 ratio

15. Alveolar Gas Equation
• PAO2 =PIO2- 1.2(PaCO2)*
• Where PAO2 isthe average alveolar PO2, and PIO2 isthe partial
pressure of inspired oxygen in the trachea
PIO2 = FIO2 (PB – 47 mm Hg)
• FIO2 isfraction of inspired oxygen and PBisthe barometric pressure.
47 mm Hg is the water vapor pressure at normal body
temperature.
* Note: Thisisthe “abbreviated version” of the AG equation,
suitable for most clinical purposes. In the longer version, the
multiplication factor “1.2” declines with increasing FIO2, reaching
zero when 100% oxygen is inhaled. In these exercises “1.2” is
dropped when FIO2 isabove 60%.

16. P(A-a)O2
• P(A-a)O2 isthe alveolar-arterial difference in partial
pressure of oxygen.
• PAO2 isalways calculated based on FIO2, PaCO2, and
barometric pressure.
• PaO2 is always measured on an arterial blood sample in
a “blood gas machine.”
• Normal P(A-a)O2 ranges from @5 to 25 mm Hg breathing
room air (it increases with age).
• A higher than normal P(A-a)O2 means the lungs are not
transferring oxygen properly from alveoli into the
pulmonary capillaries. Except for right to left cardiac
shunts, an elevated P(A-a)O2 signifies some sort of
problem within the lungs.

17. • PaO2 ….is the pressure exerted by
dissolved oxygen, not a quantity of
oxygen
• To quantify oxygen calculate CaO2

18. How much oxygen isin the blood?
PaO2 vs. SaO2 vs. CaO2
OXYGEN PRESSURE: PaO2
• Since PaO2 reflects only free oxygen molecules dissolved in plasma
and not those bound to Hb, PaO2 cannot tell us “how much”
oxygen isin the blood;
OXYGEN SATURATION: SaO2
• The percentage of all the available heme binding sites saturated
with oxygen is the Hb oxygen saturation (in arterial blood, the SaO2).
OXYGEN CONTENT: CaO2
• Only CaO2 (units ml O2/dl) tells us how much oxygen is in the blood;
this isbecause CaO2 isthe only value that incorporates the Hb
content. Oxygen content can be measured directly or calculated
by the oxygen content equation:
CaO2 = (Hbx1.34 x SaO2
) + (.003x PaO2)
Oxygen delivery =Cardiac outputx CaO2

19. Oxygen Dissociation Curve: SaO2 vs.PaO2
Also shown are CaO2 vs. PaO2 for two different hemoglobin contents: 15 gm%and
10 gm%. CaO2 units are ml O2/dl. P50 isthe PaO2 at which SaO2 is50%.
Point “X” isdiscussed on later slide.
CaO2

20. CO Does Not Affect PaO2 – Be Aware!
• Review the O2 dissociation curve shown on a previous
slide. “X” represents the 2ndset of blood gases for a
patient who presented to the ERwith headache and
dyspnea & h/o exposure to smoke in a closed room
• His first blood gases showed PaO2 80 mm Hg, PaCO2 38
mm Hg, pH 7.43. SaO2 on this first set was calculated from
the O2-dissociation curve as 97%, and oxygenation was
judged normal.
• He was sent out from the ERand returned a few hours
later with mental confusion
• Thistime both SaO2 and COHb were measured (SaO2
shown by “X”): PaO2 79 mm Hg, PaCO2 31 mm Hg, pH
7.36, SaO2 53%, carboxyhemoglobin 46%.
• CO poisoningwasmissedonthefirstsetof bloodgasesbecauseSaO2was
notmeasured!

21. Which patient ismore hypoxemic, and why?
• Patient A: pH 7.48, PaCO2 34 mm Hg, PaO2 85 mm Hg, SaO2 95%,
Hemoglobin 7 gm%
• Patient B: pH 7.32, PaCO2 74 mm Hg, PaO2 59 mm Hg, SaO2 85%,
Hemoglobin 15 gm%
• Patient A:
Arterial oxygen content = .95 x 7 x 1.34 = 8.9 mlO2/dl
• Patient B:
Arterial oxygen content = .85 x 15 x 1.34 = 17.1 mlO2/dl
• Patient A, with the higher PaO2 but the lower hemoglobin content, is
more hypoxemic.
• In this problem the amount of oxygen molecules contributed by the
dissolved fraction is negligible and will not affect the answer.

22. Assessment of acid base balance…

23. Basics
•Nano equivalent =1×10-9
•[H+]= 40 nEq/L (16 to 160 nEq/L) at pH-7.4
•For every 0.3 pH change = [H+] double

24. Very fast8
0
%in ECF
Startswithinminutes
good responseby 2hrs,
complete by 12-24hrs
Startsafterfewhrs
complete by 5-7days

25. 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
-
pH ~ ---------
PaCO2

26. Abnormal Values
pH < 7.35
• Acidosis (metabolic
and/or respiratory)
pH > 7.45
• Alkalosis (metabolic
and/or respiratory)
paCO2 > 45 mm Hg
• Respiratory acidosis
(alveolar
hypoventilation)
paCO2 < 35 mm Hg
• Respiratory alkalosis
(alveolar
hyperventilation)
HCO3 < 22meq/L
•Metabolic acidosis
HCO3 > 26meq/L
• Metabolic alkalosis

27. SIMPLEACID-BASEDISORDER
Simple acid-base disorder – a single
primary process of acidosis or alkalosis
with or with out compensation
1.pH=7.2 PCO2 = 60 mmHg, HCO3-24mEq/L-no
compensation
2.pH 7.36, PaCO2 53 ,HCO3 30-with compensation

28. Mixed Acid-base Disorders are Common
• In chronically ill respiratory patients, mixed
disorders are probably more common than
single disorders, e.g., RAc + MAlk, RAc +
Mac, Ralk + MAlk.
• In renal failure (and other conditions)
combined MAlk + MAc isalso encountered.
Clues toa mixed disorder:
• Normal pH with abnormal HCO3 or CO2
• PaCO2 and HCO3 move in opposite directions
• pH changes in an opposite direction for a
known primary disorder

29. Characteristics of  acid-base disorders
DISORDER PRIMARY
RESPONSES
COMPENSATORY
RESPONSE
Metabolic
acidosis
Metabolic
alkalosis
Respiratory
acidosis
Respiratory
alkalosis
 [H+]  PH  HCO3
-  pCO2
 [H+]  PH  HCO3
-
 pCO2
 [H+]  PH  pCO2  HCO3
-
 [H+]  PH  pCO2  HCO3
-

30. Compensation…The Rules..
The body always tries to normalize the pH
so…
• CO2 and HCO3 should rise and fall
together in simple disorders
• Compensation never overcorrects the pH
• Lack of compensation in an appropriate
time interval defines a 2nd disorder
• Compensatory responses require normally
functioning lungs and kidneys

31. Metabolic alkalosis PCO2  0.7 mmHg per 1.0 meq/L HCO3
-
1.Compensation is complete (pCO2 levels out)in 12-24
hours.
2.The limit of compensation is a pCO2 of 60 mmHg
RENAL & RESPIRATORYCOMPENSATIONS TO  ACID-
BASE DISTURBANCES
Disorder Compensatory response
Metabolic acidosis PCO2  1.2 mmHg per 1.0 meq/L HCO3
1. Compensation complete in12-24hrs
2. Limit of CO2 is10mmHg

32. Respiratory acidosis [HCO3-] 
Acute 1.0 meq/L per 10 mmHg  Pco2
Chronic 3.5 meq/L per 10 mmHg  Pco2
Respiratory alkalosis [HCO3-] 
Acute 2.0 meq/L per 10 mmHg  Pco2
Chronic 4.0 meq/L per 10 mmHg  Pco2

33. Expected changes in pH for a 10-mm Hg change in
PaCO2 resulting from either primary respiratory
acidosis or respiratory alkalosis:
ACUTE CHRONIC
• Respiratory Acidosis
pH ↓ by 0.07 pH ↓ by 0.03
• Respiratory Alkalosis
pH ↑ by 0.08 pH ↑ by 0.03

34. Anion Gap
AG = [Na+
] - [Cl-
+HCO3-
]
• Elevated anion gap represents
metabolic acidosis
• Normal value: 10 ± 2 mmol/L
• Major unmeasured anions
– albumin
– phosphates
– sulfates
– organic anions

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

36. Sixsteps for ABG ANALYSIS
• 1. The first step - Look at the pH - Label it.
pH of 7.30, PaCO2 of 80 mm Hg, and
HCO3- of 27 mEq/L.
• ACIDOSIS

37. • 2. The second step look at -pCO2. Label it.
• pH of 7.30, PaCO2 of 80 mm Hg, and
HCO3- of 27 mEq/L.
• Increased
Normal pCO2 levels
are 35-45mmHg.
Below 35 isalkalotic,
above 45 isacidic.

38. • 3. The third step isto 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 is22-26
mEq/L. If the HCO3 isbelow 22,
the patient isacidotic. If the
HCO3 isabove 26, the patient
is alkalotic

39. 4.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 ison acidotic side & PCO2 isincreased.
So it isrespiratory acidosis

40. • 5. Fifth, 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 isgoing in opposite direction of
pH. So it ismetabolic compensation

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

42. • 6. Calculate the anion gap if it ismore
there isMetabolic acidosis
AG = [Na+] - [Cl-+HCO3-]

43. • Don’t forget to assess ventilationand
oxygenation status ….

44. A patient’s in acute respiratory distress,
ABG shows pH of 7.14, PaCO2 of 70 mm
Hg, and HCO3- of 23 mEq/L. How would
you describe the likely acid-base
disorder(s)?
Example…

45. • Isthe problem only acute respiratory acidosis or isthere
some additional process?
• For every 10-mm Hg rise in PaCO2 (before any renal
compensation), pH falls about 0.07units.
• Because this patient's pH isdown by 0.26, or 0.05 more
than expected for a 30-mm Hg increase in PaCO2, there
must be an additional metabolic problem.
• Also note that with acute CO2 retention of this degree,
the HCO3- should be elevated by 3 mEq/L.
• Decreased perfusion leading to mild lactic acidosis
would explain the metabolic component.

46. Importance of History/Patients
•pH 7.08
•PCO2 80
•HCO3-24mEq/l
•80KG Man post
gastrectomy on CMV 6L
of mv
•Acidosis
•No compensation
•Expected HCO3-
24+4=28mEq/L
•pH 7.08
•PCO2 80
•HCO3-24mEq/l
•Diabetic + Chronic COPD
•Baseline PCO2 -80
•Stopped insulin few days
back
•DKA
•Expected HCO3-
=24+4×3.5=24+14=38

47. Sample ABG
• pH 7.45
• PaCO2 38
• HCO3 23
• Analysis:
• Cause:??

48. Case 1
• Mr. A is a 60 year-old with pneumonia. He is admitted
with dyspnea, fever, and chills. His blood gas is below:
pH 7.28
CO2 56
PO2 70
HCO3 25
SaO2 89%
• What isyour interpretation?
• What interventions would be appropriate for Mr. A?
• Mr. A has an uncompensated respiratory acidosis with
hypoxemia as a result of his pneumonia

49. Case 2
• Ms. Bisa 24 year-old college student. She has acute GE
and iscomplaining a of a 3 day history of watery
diarrhea. A blood gas isobtained to assess her
acid/base balance:
pH 7.28
CO2 43
pO2 88
HCO3 20
SaO2 96%
• What isyour interpretation?
• What interventions would be appropriate for Ms. B?
• Ms. Bhas an uncompensated metabolic acidosis. This is
due to excessive bicarbonate loss from her diarrhea.

50. Case 3
• Mr. C isa 80 year-old nursing home resident admitted
with urosepsis. Over the last two hours he has developed
shortness of breath and isbecoming confused. HisABG
shows the following results:
pH 7.02
CO2 55
pO2 77
HCO3 14
SaO2 89%
• What isyour interpretation?
• What interventions would be appropriate for Mr. C?
• Mr. C has a metabolic and respiratory acidosis with
hypoxemia. The metabolic acidosis iscaused by his
sepsis. The respiratory acidosis issecondary to respiratory
failure.

51. Case 4
• 4. Mrs. D isa thin, elderly-looking 61 year-old
COPD patient. She has an ABG done as part of
her routine care in the pulmonary clinic. The
results are as follows:
pH 7.37
CO2 63
pO2 58
HCO3 35
SaO2 89%
• What is your interpretation?
• What interventions would be appropriate for
Mrs. D?
• Mrs. D has a fully-compensated respiratory
acidosis with hypoxemia

52. Case 5
• Ms. Eisa 17 year-old with intractable vomiting. Shehas
some electrolyte abnormalities, so a blood gas is
obtained to assess her acid/base balance.
pH 7.50
CO2 36
pO2 92
HCO3 27
SaO2 97%
• What isyour interpretation?
• What interventions would be appropriate for Ms. E?
• Ms. Ehas an uncompensated metabolic alkalosis.

53. Case 6
• Mr. Fisa 18 year-old comatose, quadriplegic
patient who has the following ABG done as part
of a medical workup:
pH 7.44
CO2 22
pO2 96
HCO3 16
SaO2 98%
• What is your interpretation?
• What interventions would be appropriate for Mr.
F?
• His blood gas shows a fully-compensated
respiratory alkalosis

54. Case 7
• A 76 yrs, female admitted with right sided weakness, visual
disturbance, slurred speech. Started on NG feeding but has large
vomit 24 hrs later. She initially appears well later she became
agitated, distressed, pyrexial
• PEx: RS-basal coarse crepts present, CNS-confused, other findings
same as before
• PR-100/min, RR-29/min, BP-110/70 mmHg, O2%-92% with
supplementary O2 ( reservoir mask +O2)
Na+ 136 mEq/ L
K+ 3.8 mEq/L
Cl- 99 mEq/L
lactate 1.5 mmol/L
FIO2 .60
pH 7.4
PaCO2 33 mm Hg
PaO2 65 mm Hg
SaO2 92%
HCO3 21 mEq/L
-
%COHb 2.1%
Hb 13 gm%
How would you characterize her state of oxygenation, ventilation,
and acid-base balance? What is the likely diagnosis??

55. • Type I respiratory impairment, mild
respiratory alkalosis balanced by
metabolic acidosis
• Aspiration pneumonia

56. Case 8
• Mrs. H isfound 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 isobtained:
pH 6.89
CO2 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

57. Case 9
• Mr. X isin respiratory distress. He has a history of
Type-I diabetes mellitus and is now febrile. His
ABG shows:
pH 7.00
CO2 59
pO2 86
HCO3 14
SaO2 91%
• What is your interpretation?
• What interventions would be appropriate for Mr.
X?
• Mr. X has a metabolic and respiratory acidosis
with hypoxemia.

58. Case 10
• Ms. Ywas admitted for a drug overdose. She isbeing
mechanically ventilated and a blood gas is obtained to
assess her for weaning. The results are asfollows:
pH 7.54
CO2 19
pO2 100
HCO3 16
SaO2 98%
• What isyour interpretation?
• What interventions would be appropriate for Ms. Y?
• Mrs. Yisbeing overventilated which caused a partially-
compensated respiratory alkalosis

59. Case 11
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 isbreathing oxygen through a
nasal cannula at 3 l/min.
pH
PaCO2
%COHb
PaO2
SaO2
Hb
HCO3
-
CaO2
7.41
20 mm Hg
1.0%
80 mm Hg
95%
13.3 gm%
12 mEq/L
17.2 ml O2/dl
How would you characterize his state of oxygenation,
ventilation, and acid-base balance?

60. • Normal pH with very low bicarbonate and
PaCO2 indicates combined respiratory
alkalosis and metabolic acidosis.

61. Case 12
• A 59 yrs, male, chronic alcoholic, h/o severe upper
abdominal pain x 3 days, breathlessness present,
excessive alcohol consumption for past few weeks
• PEx: looks sick, shortness of breath present, epigastric tenderness
present, CXR- few b/l scatteredopacites
• PR-120/min, RR-28/min, BP-75/60 mmHg, O2%-98%
• On 8 l/min O2 with mask & reservoir bag
Na+ 142 mEq/L
K+ 3.9 mEq/L
Cl- 101 mEq/L
lactate 4mmol/L
iCa+ 0.8 mmol/L
Hb
pH
PaCO2
PaO2
SaO2
HCO3
-
BE
11 gm%
7.31
24 mm Hg
81 mm Hg
98%
15 mEq/L
-12 mEq/L
How would you characterize his state of oxygenation, ventilation,
and acid-base balance? What is the probable diagnosis and furhter
action ??

62. • Type I respiratory impairment, severe
metabolic acidosis with partial
compensation most likely due to acute
pancreatitis

63. • A 55 yr, female c/o sudden onset of breathlessness & left sided chest
pain, underwent knee replacement operation 4 days back, no
relevant past medical history
• PEx: slight shortness of breath, CVS/RS-NAD, no clinical evidence of
DVT, CXR-NAD, ECG-only tachycardia
• PR-98/min, RR-20/min, BP-150/90 mmHg, temp-36.6 degrees,O2%-
99%
Case 13
Na+ 136 mEq/ L
K+ 3.8 mEq/L
Cl- 99 mEq/L
lactate 1 mmol/L
FIO2 .21
pH 7.43
PaCO2 37 mm Hg
PaO2 91 mm Hg
SaO2 99%
HCO3 25.8 mEq/L
-
%COHb 2.1%
Hb 10 gm%
How would you characterize his state of oxygenation, ventilation,
and acid-base balance? Does she require any further work up??

64. • Normal gas exchange, normal acid base status
• PA02=(.21 x 713) + (37 x 1.2), PaO2 91 mm Hg
• P(A-a)02= 106-91=15 mmHg
• Patient ishigh risk for PE
• Normal ABG never excludes it and she requires
V/Q scan or CTPA

65. Case 14
• A 36 yr, male with alprazolam tab consumption x 3,
slightly drowsy but easily arousable, no relevant past
medical history
• PEx: RS/CVS-NAD
• PR-80/min, RR-14/min, BP-110/70 mmHg, temp-36.6 degrees,
SpO2%-99%
Na+ 138 mEq/L
K+ 3.8 mEq/L
Cl- 104 mEq/L
lactate 1 mmol/L
FIO2 .21
pH 7.37
PaCO2 41 mm Hg
PaO2 40 mm Hg
SaO2 74%
HCO3 24 mEq/L
-
%COHb 2.1%
Hb 13 gm%
How would you characterize his state of oxygenation, ventilation,
and acid-base balance? What isthe likely explanation for low
PaO2??

66. • Appearance of severe type I respiratory failure,
normal acid base status
• There ismarked discrepancy between SaO2by
pulse oximeter and that calculated by ABG
• It is a venous sample & repeat ABG should be
done

67. Case 15
• A 70 yrs, male, comes to casualty with shortness of breath
and excessive tiredness, h/o chronic PR bleeding present
• Past medical history-k/c/o HTN,IHD
• PEx: RS/CVS-NAD
• PR-110/min, RR-23/min, BP-140/90 mmHg, O2%-99% on air
Na+ 138 mEq/L
K+ 3.8 mEq/L
Cl- 104 mEq/L
lactate 1 mmol/L
FIO2 .21
pH 7.49
PaCO2 25 mm Hg
PaO2 89 mm Hg
SaO2 99%
HCO3 22 mEq/L
-
%COHb 2.1%
Hb 6.7 gm%
How would you characterize his state of oxygenation, ventilation,
and acid-base balance? What isthe likely explanation for
breathlessness??

68. • Hyperventilation- no impairment of oxygenation
but hypoxemia due to anaemia
• Uncompensated respiratory alkalosis
• Patient has severe anaemia due to iron
deficiency/chronic rectal bleeding

69. Case 16
• A 21yrs,female, known asthmatic, with 6hr h/o worsening
breathlessness & wheeze, no relief from salbutamol
inhaler
• PEx: tachypnoeic, using accessory muscles, just
managing to speak in full sentences
• PR-115/min, RR-30/min, BP-110/80 mmHg, O2%-96% on air
Na+ 138 mEq/L
K+ 3.8 mEq/L
Cl- 104 mEq/L
lactate 1 mmol/L
FIO2
pH
PaCO2
PaO2
SaO2
HCO3-
Hb
.21
7.38
43 mm Hg
76 mm Hg
96%
24 mEq/L
12 gm%
How would you characterize her state of oxygenation, ventilation,
and acid-base balance? Would you be concerned?? If so why??

70. • Mild type I respiratory impairment
• PaCO2-high end of the normal range
• Life threatening attack

71. Treat the patient not the ABG!!!
• “ABG’’ should supplement clinical judgment not
substitute it”
• Treat the underlying clinical condition(s); this will
usually suffice to correct most acid-base
disorders.
• If there is concern that acidemia or alkalemia is
life-threatening, aim toward correcting pH into
the range of 7.30 - 7.52 ([H+] = 50-30 nM/L).

72. • THANK YOU FOR PATIENT HEARING…

73. A patient is admitted to the ICU with the
following lab values:
BLOOD GASES
pH: 7.40
PCO2: 38
HCO3: 24
PO2: 72
ELECTROLYTES,BUN & CREATININE
Na: 149
K: 3.8
Cl: 100
CO2: 24
BUN: 110
Creatinine: 8.7
What is(are) the acid-base disorder(s)?
(in this case venous CO2=arterial HCO3-)

74. Step 1: Anion gap
AG = Na+ - (Cl + CO2)= 149 - (100 + 24) = 25
This high an AG indicates an anion gap metabolic acidosis.
Step 2: Delta anion gap
calculated AG= 25mEq/L
normal AG = 12mEq/L
25 - 12 = 13 mEq/L; this isthe excess or delta anion gap
Step 3: Delta serum CO2 = normal CO2 - measured CO2
=27 (average normal venous CO2) - 24 = 3 mEq/L
Step 4: Bicarbonate Gap = delta AG - delta CO2 = 13 - 3 =
10 mEq/L
Thismeans the measured bicarbonate is10 mEq/Lhigher
than expected from the excess AG, indicating (in this
case) a metabolic alkalosis. Thus this patient, with normal
pH and PaCO2, has BOTH metabolic acidosis and
metabolic alkalosis. The patient was both uremic
(causing metabolic acidosis) and had been vomiting
(metabolic alkalosis)

75. pH < 7.35
Acidosis
pH > 7.35
Alkalosis
pCO2 > 40
Respiratory
HCO3 < 24
Metabolic
pCO2 < 40
Respiratory
HCO3 > 24
Metabolic
PaCO2 ↓10
→HCO3 ↓4
PaCO2 ↓10
→HCO3 ↓2
PaCO2 ↑7
→HCO3 ↑10
Urine Cl < 10
Cl Responsive
Anion Gap < 12
Non-Anion Gap
Anion Gap > 12
Anion Gap
Urine Cl > 10
Cl Unresponsive
Interpreting ABGs
Osm Gap > 10
Methanol
Ethylene Glycol
Osmolar Gap < 10
Ketoacidosis
Lactic acidosis
Uremia
Aspirin/salicylate tox
Diarrhea
Renal tubular acidosis
Acetazolamide
Total parenteral nutrition
Ureteral diversion
Pancreas transplant
CNS depressants
Neuromuscular disorder
Thoracic cage abnormalities
Obstructive lung disease
Obesity/hypoventilation syndrome
Myxedema coma
Anxiety/pain
Sepsis
CNS (stroke)
Aspirin OD
Chronic liver disease
Pulmonary embolism
Pregnancy
Hyperthyroidism
Loss of body fluids:
Vomiting
Nasogastric suctioning
Diuretic use
Excess body fluids:
Exogenous steroids
Cushing’s syndrome
Hyperaldosteronism
Bartter’s syndrome
=Na - (Cl+HCO3)
Acute
PaCO2 ↑10
→HCO3 ↑1
Chronic
PaCO2 ↑10
→HCO3 ↑4
PaCO2 ↓12
→HCO3 ↓10
Compensation:
If:
ΔPCO2/ΔHCO3
=
CO2/HCO3ratio
Then it is comp.
Acute
Chronic
(2xNa) + (Glu/18) +
(BUN/2.8) = calculated
serum osmoles
HCO3 loss Extra H+

76. P(A-a)O2: Test Your Understanding - Answers
• a) PAO2 = .40 (760 - 47) - 1.2 (50) = 225 mm Hg; P(A-a)O2 = 225 - 150
= 75 mm Hg
The P(A-a)O2 is elevated but actually within the expected range for
supplemental oxygen at 40%, so the patient may or may not have
a defect in gas exchange.
• b) PAO2 = .28 (713) - 1.2 (75) = 200 - 90 = 110 mm Hg; P(A-a)O2 =
110 - 95 = 15 mm Hg
Despite severe hypoventilation, there is no evidence here for lung
disease. Hypercapnia ismost likely a result of disease elsewhere in
the respiratory system, either the central nervous system or chest
bellows.
• c) PAO2 = .21 (713) - 1.2 (15) = 150 - 18 = 132 mm Hg; P(A-a)O2 =
132 - 120 = 12 mm Hg
Hyperventilation can easily raise PaO2 above 100 mm Hg when the
lungs are normal, as in thiscase.

77. d) PAO2 = .80 (713) - 40 = 530 mm Hg (Note that the factor 1.2
isdropped since FIO2 isabove 60%)
P(A-a)O2 = 530 - 350 = 180 mm Hg
P(A-a)O2 is increased. Despite a very high PaO2, the lungs
are not transferring oxygen normally.
e) PAO2 = .21 (713) - 1.2 (72) = 150 - 86 = 64 mm Hg; P(A-a)O2 =
64 - 80 = -16 mm Hg
A negative P(A-a)O2 isincompatible with life (unless it isa
transient unsteady state, such as sudden fall in FIO2 -- not
the case here). In this example, negative P(A-a)O2 can be
explained by any of the following: incorrect FIO2, incorrect
blood gas measurement, or a reporting or transcription
error.
P(A-a)O2: Test Your Understanding - Answers

78. PaCO2 and Alveolar Ventilation: Q & A
1. What is the PaCO2 of a patient with respiratory
rate 24/min, tidal volume 300 ml, dead space
volume 150 ml, CO2production 300 ml/min? The
patient shows some evidence of respiratory distress.
First, you must calculate the alveolar ventilation.
Since minute ventilation is24 x 300 or 7.2 L/min, and
dead space ventilation is24 x 150 or 3.6 L/min,
alveolar ventilation is3.6 L/min. Then
300ml/minx.863
PaCO2=-----------------------
3.6L/min
PaCO2 =71.9mmHg

79. Alveolar Gas Equation
PAO2=PIO2
- 1.2(PaCO2)
where PIO2 = FIO2 (PB – 47 mm Hg)
Except in a temporary unsteady state, alveolar PO2
(PAO2) isalways higher than arterial PO2 (PaO2). As a
result, whenever PAO2 decreases, PaO2 also decreases.
Thus, from the AG equation:
• If FIO2 and PBare constant, then as PaCO2increases both
PAO2 and PaO2 will decrease (hypercapnia causes
hypoxemia).
• If FIO2 decreases and PBand PaCO2are constant, both
PAO2 and PaO2 will decrease (suffocation causes
hypoxemia).
• If PBdecreases (e.g., with altitude), and PaCO2 and FIO2
are constant, both PAO2 and PaO2 will decrease
(mountain climbing leads to hypoxemia).

80. Alveolar Gas Equation:
Q & A
1. What isthe PAO2 at sea level in the following
circumstances? (Barometric pressure = 760 mm Hg)
a) FIO2= 1.00, PaCO2 = 30 mm Hg
b) FIO2= .21, PaCO2 = 50 mm Hg
c) FIO2= .40, PaCO2 = 30 mm Hg
To calculate PAO2 the PaCO2 must be subtracted from
the PIO2. Again, the barometric pressure is760 mm Hg
since the values are obtained at sea level. In part a,
the PaCO2 of 30 mm Hg isnot multiplied by 1.2 since
the FIO2is 1.00. In parts b and c, PaCO2 is multiplied by
the factor 1.2.
a) PAO2 = 1.00 (713) - 30 = 683 mm Hg
b) PAO2 = .21 (713) - 1.2 (50) = 90 mm Hg
c) PAO2 = .40 (713) - 1.2 (30) = 249 mm Hg

81. Ventilation-perfusion Imbalance
• A normal amount of ventilation-perfusion (V-Q)
imbalance accounts for the normal P(A-a)O2.
• By far the most common cause of low PaO2 isan
abnormal degree of ventilation-perfusion imbalance
within the hundreds of millions of alveolar-capillary units.
Virtually all lung disease lowers PaO2 via V-Q imbalance,
e.g., asthma, pneumonia, atelectasis, pulmonary
edema, COPD.
• Diffusion barrier is seldom a major cause of low PaO2 (it
can lead to a low PaO2 during exercise).

82. Respiratory and Renal Compensatory
Mechanisms for ACID-BASE Disturbance

83. Quantification of Dead space
VD
=
VT
25-40% is normal
In MV pts till 55% isnormal
More than 60% isabnormal
dead space
Volume not taking
part in gas
exchange=dead
space
Effective alveolar
ventilation
=MV-VD

84. PCO2 vs. Alveolar Ventilation
The relationship isshown for
metabolic CO2 production rates
of 200 ml/min and 300 ml/min
(curved lines).
A fixed decrease in VA(x-axis) in
the hypercapnic patient will
result in a greater rise in PaCO2
(y-axis) than the same VA
change when PaCO2 islow or
normal.
This graph also shows that if VA is
fixed, an ↑ in CO2 production will
result in an ↓ in PaCO2.

85. Problems: Oxygenation
• Room Air, PaO2 = 45, PaCO2 =30
–PAO2 = 150 – 1.2(30) = 114 mm Hg
– P(A-a)O2 = 114 - 45 = 69 elevated
• Now on 100% O2, PaO2 = 65, PaCO2= 32
– minimal elevation in PaO2
– shunt major cause of hypoxemia

86. Problems: Oxygenation
• Room Air, PaO2 = 45, PaCO2 =45
–PAO2 = 150 - 1.2(45) = 96
–P(A-a)O2 = 96 - 45 = 51
• Now on 100% O2, PaO2 =555, PaCO2 = 48
–PAO2 = 1.0(760 - 47) - 1.2(48) =655
–P(A-a)O2 = 655 - 555 = 100
– Dramatic increase in PaO2
– V/Q mismatch major cause of hypoxemia

87. Respiratory/Metabolic