This document discusses oxygenation and ventilation monitoring techniques including indices of oxygenation such as pulse oximetry and capnography. It provides details on how to interpret pulse oximetry readings and capnography waveforms. Common abnormalities in capnography waveforms are described along with their potential causes. The uses of capnography in intubated and non-intubated patients are outlined. Arterial blood gases and the steps to analyze them are also reviewed.

1. OXYGENATION &
VENTILATION
MONITORING

2. Point of Discussion
1. Indices of oxygenation
2. Indices of ventilation
3. Pulse oximetry
4. Capnography
5. Arterial and venous blood gases

3. Indices of Oxygenation

4. Alveolar Arterial O2 Gradient
Alveolar Gas Capillary Blood
initial Initial
Thickness
A-a Gradient

5. Pulse Oximetry

6. O2-Hg Dissociation Curve
PaO2 (mm Hg)
90
60

7. Sources of error
 Poor peripheral perfusion
 Dark skin
 False nails or nail varnish
 Lipaemia
 Bright ambient light
 Poorly adherent probe
 Excessive motion
 Carboxyhaemoglobin or methaemoglobin

8. The Ventilation Vital Sign
Capnography

9. Capnograhy vs Capnometry?
 Capnography- Continuous analysis and
recording of Carbon Dioxide concentrations in
respiratory gases ( I.E. waveforms and
numbers)
 Capnometry- Analysis only of the gases no
waveforms

10. Semi-Quantitative Capnometry
 Relies on pH change
 Paper changes color
 Purple to Brown to Yellow

11. Quantitative Capnometry
 Absorption of infra-
red
light
 Gas source
 Side Stream
 In-Line
Factors in choosing
device:
 Warm up time
 Cost
 Portability

12. Waveform Capnometry
 Adds continuous
waveform display to
the ETCO2 value.
 Additional
information in
waveform shape
can provide clues
about causes of
poor oxygenation.

13. Why ETCO2 I Have my Pulse
Ox?
Oxygen Saturation
Reflects
Oxygenation
SpO2 changes lag
when patient is
hypoventilating or
apneic
Should be used with
Capnography
Carbon Dioxide
Reflects Ventilation
Hypoventilation/Apn
ea detected
immediately
Should be used with
pulse Oximetry
Pulse Oximetry Capnography

14. What does it really do for me?
Bronchospasms:
Asthma, COPD,
Anaphlyaxis
Hypoventilation:
Drugs, Stroke, CHF,
Post-Ictal
Shock & Circulatory
compromise
Hyperventilation
Syndrome:
Biofeedback
Verification of ETT
placement
ETT surveillance during
transport
Control ventilations
during CHI and
increased ICP
CPR: compression
efficacy, early signs of
ROSC, survival predictor
Non-Intubated Applications Intubated Applications

15. NORMAL CAPNOGRAM
Phase I Phase IIIPhase II
Inspiratory PhaseExpiratory Phase
70
60
50
40
30
20
10
0
PetCO2
Time
mm Hg
Phase I: anatomical dead space
Phase II : alveolar gas begins to
mix with the dead space gas
Phase III: elimination
of CO2 from the
alveoli
Phase IV

16. ABNORMALITIES
Abnormality Indication
Increased Phase III slope Obstructive lung disease
Phase III dip Spontaneous respiratio
Horizontal Phase III with large
ET-art CO2 change
Pulmonary embolism
 cardiac output
Hypovolemia
Sudden  in ETCO2 to 0 Dislodged tube
Vent malfunction
ET obstruction
Sudden  in ETCO2 Partial obstruction
Air leak
Exponential  Severe hyperventilation
Cardiopulmonary event

17. ABNORMALITIES
Abnormality Indication
Sudden increase in ETCO2 Sodium bicarb administration
Release of limb tourniquet
Gradual  Hyperventilation
Decreasing temp
Gradual  in volume
Increased baseline Rebreathing
Exhausted CO2 absorber
Gradual increase Fever
Hypoventilation

18. USES
 Metabolic
 Assess energy expenditure
 Cardiovascular
 Monitor trend in cardiac output
 Can use as an indirect Fick method, but actual
numbers are hard to quantify
 Measure of effectiveness in CPR
 Diagnosis of pulmonary embolism: measure
gradient

19. PaCO2-PetCO2 gradient
 Usually <6mm Hg
 PetCO2 is usually less
 Difference depends on the number of
underperfused alveoli
 Tend to mirror each other if the slope of Phase III
is horizontal or has a minimal slope
 Decreased cardiac output will increase the
gradient
 The gradient can be negative when healthy lungs
are ventilated with high TV and low rate
 Decreased FRC also gives a negative gradient by
increasing the number of slow alveoli

20. LIMITATIONS
 Critically ill patients often have rapidly
changing dead space and V/Q mismatch
 Higher rates and smaller TV can increase the
amount of dead space ventilation
 High mean airway pressures and PEEP
restrict alveolar perfusion, leading to falsely
decreased readings
 Low cardiac output will decrease the reading

21. PULMONARY USES
 Effectiveness of therapy in bronchospasm
 Monitor PaCO2-PetCO2 gradient
 Worsening indicated by rising Phase III without
plateau
 Find optimal PEEP by following the gradient.
Should be lowest at optimal PEEP.
 Can predict successful extubation.
 Dead space ratio to tidal volume ratio of >0.6 predicts
failure. Normal is 0.33-0.45
 Limited usefulness in weaning the vent when
patient is unstable from cardiovascular or
pulmonary standpoint
 Confirm ET tube placement

22. NORMAL Waveform
70
60
50
40
30
20
10
0 Time
mm Hg
• Square box waveform
• ETCO2 35-45 mm Hg
• Management: Monitor Patient

23. Sudden  in ETCO2 to 0
70
60
50
40
30
20
10
0 Time
mm Hg
• Loss of waveform
• Loss of ETCO2 reading
• Dislodged tube
• ET obstruction
• Management: Replace ETT

24. Esophageal Intubation
70
60
50
40
30
20
10
0 Time
mm Hg
• Absence of waveform
• Absence of ETCO2
• Management: Re-Intubate

25. CPR
70
60
50
40
30
20
10
0 Time
mm Hg
• Square box waveform
• ETCO2 15-20 mm Hg with adequate CPR
• ETCO2 falls bellow 10 mm Hg
• Management: Change Rescuers

26. Return of Spontaneous
Circulation
70
60
50
40
30
20
10
0 Time
mm Hg
• During CPR sudden increase of ETCO2 above
10-15 mm Hg
• Management: Check for pulse

27. Gradual Decrease in ETCO2
70
60
50
40
30
20
10
0 Time
mm Hg
• Hyperventilation
• Decreasing temp
• Gradual  in volume

28. Hyperventilation
70
60
50
40
30
20
10
0 Time
mm Hg
• Shortened waveform
• ETCO2 < 35 mm Hg
• Management: If conscious gives biofeedback. If ventilating
slow ventilations

29. Gradual Increase in ETCO2
70
60
50
40
30
20
10
0 Time
mm Hg
• Fever
• Hypoventilation

30. Hypoventilation
70
60
50
40
30
20
10
0 Time
mm Hg
• Prolonged waveform
• ETCO2 >45 mm Hg
• Management: Assist ventilations

31. Rising Baseline
70
60
50
40
30
20
10
0 Time
mm Hg
• Patient is re-breathing CO2
• Management: Check equipment for adequate oxygen flow
• If patient is intubated allow more time to exhale

32. Curare Cleft
70
60
50
40
30
20
10
0 Time
mm Hg
• Curare Cleft is when a neuromuscular blockade
wears off
• The patient takes small breaths that causes the cleft
• Management: Consider neuromuscular blockade re-
administration

33. Breathing around ETT
70
60
50
40
30
20
10
0 Time
mm Hg
• Angled, sloping down stroke on the waveform
• In adults may mean ruptured cuff or tube too small
• Management: Assess patient, Oxygenate, ventilate and
possible re-intubation

34. Obstructive Airway
70
60
50
40
30
20
10
0 Time
mm Hg
• Shark fin waveform
• With or without prolonged expiratory phase
• Can be seen before actual attack
• Indicative of Bronchospasm( asthma, COPD, allergic reaction)

35. Oscillation in Inspiratory Phase
70
60
50
40
30
20
10
0 Time
mm Hg
J Int Care Med, 12(1): 18-32, 1997J Int Care Med, 12(1): 18-32, 1997

36. Oscillation in Inspiratory Phase
70
60
50
40
30
20
10
0 Time
mm Hg
J Int Care Med, 12(1): 18-32, 1997J Int Care Med, 12(1): 18-32, 1997

37. Oscillation and slow Inspiration
70
60
50
40
30
20
10
0 Time
mm Hg
J Int Care Med, 12(1): 18-32, 1997J Int Care Med, 12(1): 18-32, 1997

38. 6 Step ABG’s Analysis
Blood Gases

39. 1. Acidemic/Alkalemic?
 This refers to the pH
 Normal pH= 7.40 ± 0.05
 Acidemia pH < 7.40
 Alkalemia pH > 7.40
 Normal PaCO2 = 40 ± 5 (35-45)
 Normal HCO3 = 24 ± 2 (22-26)

40. 2. Primary -osis
pH emia PaCO2 HCO3 1 ° osis
<7.40 acidemia <40 <24 1°Metabol
ic
acidosis
<7.40 acidemia >40 >24 Respirato
ry
acidosis
>7.40 alkalemia >40 >24 Metabolic
alkalosis
>7.40 alkalemia <40 <24 Respirato
ry
alkalosis

41. 2. Respiratory process acute or
chronic ?
 Respiratory Acidosis Acute :
∆ pH= 0.08x(PaCO2-40)/10
 Respiratory Acidosis Chronic :
∆ pH= 0.03x(PaCO2-40)/10
 Respiratory Alkalosis Acute :
∆ pH= 0.08 x (40-PaCO2)/10
 Respiratory Alkalosis Chronic :
∆ pH= 0.03 x (40-PaCO2)/10

42. 4. Metabolic acidosis
 Anion gap vs. Nongap acidosis
 Anion gap (AG) = Na-Cl-HCO3

43. 3. Adequate degree of
compensation for Metabolic
Acidosis ?
 Calculated (expected) PaCO2 for Gap
acidosis (Winte r’s fo rm ula )
 Calculated PaCO2=(1.5 x HCO3) +8±2
 Measured PaCO2>Calculated PaCO2 then
concomitant re spirato ry acido sis
 Measured PaCO2<Calculated PaCO2 then
concomitant re spirato ry alkalo sis

44. 4. Calculated (expected) HCO3
 Calculated (expected) HCO3 =
(Pt.’s AG-nl gap) + measured HCO3
 Calculated HCO3>30 associated metabolic
alkalosis
 Calculated HCO3<23 associated nongap
metabolic acidosis
 AKA Delta Delta ∆ ∆

45. 4. Metabolic acidosis
 Check for Osmolar gap (OG)
OG:Measured osmol – Calculated > 10
Calculated Osmol=
(2xNa) + glucose/18 + BUN/2.8 +ethanol/4.6

46. 5. Calculate Urinary AG
 Determines renal vs. extrarenal causes
 UAG=UNa+UK-UCl (nl -10 to 10).
 UAG <-10 = extrarenal b/c kidneys making a lot
of NH3Cl to buffer acidosis
 UCl nl/high (>40) AKA saline unre spo nsive
 UAG> 10 = renal b/c kidneys unable to make
NH3Cl to excrete acid.
 UCl low (<25) saline re spo nsive

47. 6. Adequate degree of compensation for Metabolic
Alkalosis ?
For every ∆ 1 in HCO3 the paCO2 ∆ 0.6

48. Adequate degree of compensation ?
PrimaryPrimary
problemproblem
CompensationCompensation For everyFor every
∆∆ inin
ExpectedExpected
∆∆
Metabolic AcidosisMetabolic Acidosis Respiratory alkalosisRespiratory alkalosis
11 ↓↓ HCO3HCO3 PaCO2PaCO2 ↓↓ 1.21.2
Metabolic AlkalosisMetabolic Alkalosis Respiratory acidosisRespiratory acidosis
11 ↑↑ HCO3HCO3 PaCO2PaCO2 ↑↑ 0.60.6
RespiratoryRespiratory
Acidosis AcuteAcidosis Acute
Metabolic AlkalosisMetabolic Alkalosis
11 ↑↑ PaCO2PaCO2 HCO3HCO3 ↑↑ 0.10.1
RespiratoryRespiratory
Acidosis ChronicAcidosis Chronic
Metabolic AlkalosisMetabolic Alkalosis
11 ↑↑ PaCO2PaCO2 HCO3HCO3 ↑↑ 0.40.4
RespiratoryRespiratory
Alkalosis AcuteAlkalosis Acute
Metabolic AcidosisMetabolic Acidosis
11 ↓↓ PaCO2PaCO2 HCO3HCO3 ↓↓ 0.20.2
RespiratoryRespiratory
Alkalosis ChronicAlkalosis Chronic
Metabolic AcidosisMetabolic Acidosis
11 ↓↓ PaCO2PaCO2 HCO3HCO3 ↓↓ 0.40.4

49. ABG Problems:
145145 100100 1616
4.04.0 1212 1.01.0
 7.2/26/85/95% on
RA

50. Answer
 Metabolic acidosis
 145-100-12=AG 33
 Expected PaCO2 1.5x12 +8 ±2=26±2
appropriate
 Expected HCO3= (33-12) + 12 =33
 Concomitant metabolic alkalosis

51. ABG Problems
 7.1/35/60/90% on
RA
135135 106106 1616
4.24.2 1010 1.01.0

52. Answer
 Metabolic acidosis
 135-106-10 = AG 19
 Expected PaCO2 1.5 x 10 +8 ±2=23±2
Measured >calculated
 Concomitant respiratory acidosis
 Expected HCO3 = 19-12 +10 = 17
 Concomitant nongap metabolic acidosis
 Next calculate UAG

53. ABG Problems
 HIV, HBV associated ESLD, ARF with pleural
effusions, tachypneic RR 34
 7.48/28/55/90% on 4L NC
155|97|41/117
4.7| 18|1.7

54. Answer
Respiratory alkalosis
∆ H:748-740=8
∆ paCO2: 40-28=12
8/12=0.67 Acute on chronic respiratory alkalosis.
Acute from tachypnea chronic from ESLD
 7.47/18/98 on 50% face mask