Transcript Document 7146587

Blood Gases and Related Tests
RET 2414
Pulmonary Function Testing
Module 6.0
Objectives

Describe how pH and PCO2 are used to assess acid-
base balance

Interpret PO2 and oxygen saturation to assess
oxygenation

Identify the correct procedure for obtaining an
arterial blood gas specimen

List situation in which pulse oximetry can be used to
evaluate a patient’s oxygenation
Objectives

Describe the use of capnography to assess changes
in ventilatory-perfusion patterns of the lung

Describe at least two limitation of pulse oximetry
Reasons for Obtaining an ABG

Assessment of ventilatory status

Assessment of acid-base balance

Assessment of arterial oxygenation
Acid – Base Balance
The maintenance of cellular function
depends on an exacting environment.
One of the most important
environmental factors is the hydrogen
ion concentration (H+), commonly
expressed as pH.
Acid – Base Balance
The pH is a function of the relation of
HCO3- (base) to PCO2 (acid) in the
blood in the following fashion:
pH ~ HCO3- (base) ~ metabolic component ~ kidney ~ 20
CO2 (acid)
respiratory component
lungs
1
Normal pH
7.40
Acid – Base Balance

Acidemia;
an acidic condition of the blood
pH < 7.35

Alkalemia; an alkaline condition of the blood
pH >7.45
Acid – Base Balance

Respiratory Component (PCO2)
Tissues
Plasma
CO2
Red Blood Cell
CO2
dCO2
H2CO3
Acid – Base Balance

Excretion of CO2 is one of the lungs
main functions
PA CO2
40 mmHg
PvCO2
PaCO2
46 mmHg
40 mmHg
Pc CO2
Acid – Base Balance

Respiratory Component (PCO2)
Ventilation
PCO2
pH
“Respiratory Acidosis”
Acid – Base Balance

Respiratory Component (PCO2)
Ventilation
PCO2
pH
“Respiratory Alkalosis”
Acid – Base Balance

Metabolic Component (HCO3- and BE)

Bicarbonate (HCO3-) is the primary blood
base and is regulated by the kidneys and
not the lungs.
Normal HCO3-
24 mEq/L
Acid – Base Balance

Metabolic Component (HCO3- and BE)

Base Excess (BE) is a measure of
metabolic alkalosis or metabolic acidosis
expressed as the mEq of strong acid or
strong alkali required to titrate one liter of
blood to a pH of 7.40
Normal B.E.
-2 to +2 mEq/L
Acid – Base Balance

Metabolic Component (HCO3- and BE)
HCO3- or B.E.
“Metabolic Acidosis”
Acid – Base Balance

Metabolic Component (HCO3- and BE)
HCO3- or B.E.
“Metabolic Alkalosis”
Acid – Base Balance

Combined Respiratory / Metabolic
Respiratory and metabolic component
moving toward the same acid/base status
PCO2
HCO3- = Acidosis
PCO2
HCO3- = Alkalosis
Acid – Base Balance

Compensation
Abnormal pH is returned toward normal by
altering the component NOT primarily
affected, i.e., if PCO2 is high, HCO3- is
retained to compensate
PCO2
HCO3-
HCO3-
PCO2
Acid – Base Balance
Normal metabolism produces
approximately 12,000 mEq of
hydrogen ions per day. Less than
1% is excreted by the kidneys,
because the normal metabolite is
CO2; which is excreted by the
lungs.
Acid – Base Balance
Acid-Base imbalance is not lifethreatening for several hours to
days following renal shutdown but
becomes critical within minutes
following cessation of breathing.
Normal Values
pH
7.40
PCO2 (mmHg)
40
HCO3- (mEq/L)
24
Acceptable Ranges
pH
(2 SD)
PCO2
HCO3-
35 – 45
22 - 26
Normal
7.35 – 7.45
Acidotic
<7.35
>45
<22
Alkalotic
>7.45
<35
>26
Arterial Oxygenation


Tissue hypoxemia exists when cellular
oxygen tensions are inadequate to meet
cellular oxygen demands.
PaO2 has become the primary tool for
clinical evaluation of the arterial
oxygenation status.
Arterial Oxygenation

Hypoxemia; an arterial oxygen tension
(PaO2) below an acceptable range.
Arterial Oxygen Tensions for Adult and Child
Normal
Acceptable Range
Hypoxemia
97 mm Hg
≥80 mm Hg (range decreases with age)
<80 mm Hg
Systematic Interpretation

Assessment of ventilatory status

Assessment of acid-base balance

Assessment of arterial oxygenation
Exercise 1
Acceptable Range
7.35 - 7.45
35 - 45
22 - 26
-2 - +2
>80
ABG Result
pH
PCO2
HCO3BE
PO2
7.26
56
24
-4
50
Acute ventilatory failure with hypoxemia
(Acute respiratory acidosis with hypoxemia)
Exercise 2
Acceptable Range
7.35 - 7.45
35 - 45
22 - 26
-2 - +2
>80
ABG Result
pH
PCO2
HCO3BE
PO2
7.56
29
24
+3
90
Acute alveolar hyperventilation without hypoxemia
(Acute respiratory alkalosis without hypoxemia)
Exercise 3
Acceptable Range
7.35 - 7.45
35 - 45
22 - 26
-2 - +2
>80
ABG Result
pH
PCO2
HCO3BE
PO2
7.56
44
38
+14
75
Uncompensated metabolic alkalosis with hypoxemia
Exercise 4
Acceptable Range
7.35 - 7.45
35 - 45
22 - 26
-2 - +2
>80
ABG Result
pH
PCO2
HCO3BE
PO2
7.20
38
15
-13
90
Uncompensated metabolic acidosis without hypoxemia
Exercise 5
Acceptable Range
7.35 - 7.45
35 - 45
22 - 26
-2 - +2
>80
ABG Result
pH
PCO2
HCO3BE
PO2
7.45
20
16
-7
90
Chronic alveolar hyperventilation without hypoxemia
(Compensated respiratory alkalosis without hypoxemia)
Exercise 6
Acceptable Range
7.35 - 7.45
35 - 45
22 - 26
-2 - +2
>80
ABG Result
pH
PCO2
HCO3BE
PO2
7.42
72
46
+18
45
Chronic ventilatory failure with hypoxemia
(Compensated respiratory acidosis with hypoxemia)
Exercise 6
A 76-year-old man with a long history of
symptomatic COPD entered the hospital with
basilar pneumonia. He was alert, oriented, and
cooperative.
Acceptable Range
7.35 - 7.45
35 - 45
22 - 26
-2 - +2
>80
ABG Result
pH
PCO2
HCO3BE
PO2
7.58
45
42
+17
38
Exercise 6
Acceptable Range
7.35 - 7.45
35 - 45
22 - 26
-2 - +2
>80
ABG Result
pH
PCO2
HCO3BE
PO2
7.58
45
42
+17
38
Question:
Is this uncompensated metabolic alkalosis with
severe hypoxemia?
Exercise 6
Acceptable Range
7.35 - 7.45
35 - 45
22 - 26
-2 - +2
>80
ABG Result
pH
PCO2
HCO3BE
PO2
7.58
45
42
+17
38
Uncompensated metabolic alkalosis with severe
hypoxemia?
Exercise 6
Acceptable Range
7.35 - 7.45
35 - 45
22 - 26
-2 - +2
>80
ABG Result
pH
PCO2
HCO3BE
PO2
7.58
45
42
+17
38
A metabolic alkalosis with hypoxemia must be
clinically correlated because a disease process
causing metabolic alkalosis would not be expected
to produce severe hypoxemia.
Exercise 6
Acceptable Range
7.35 - 7.45
35 - 45
22 - 26
-2 - +2
>80
ABG Result
pH
PCO2
HCO3BE
PO2
7.58
45
42
+17
38
Correct Interpretation:
Acute alveolar hyperventilation (respiratory
alkalosis) superimposed on chronic hypercapnia
(chronic ventilatory failure) with severe hypoxemia.
Exercise 7
A 67-year-old man admitted to the Emergency
Department with exacerbated COPD. He was
alert, oriented, and cooperative.
Acceptable Range
7.35 - 7.45
35 - 45
22 - 26
-2 - +2
>80
ABG Result
pH
PCO2
HCO3BE
PO2
7.25
90
38
+12
34
Exercise 7
Acceptable Range
7.35 - 7.45
35 - 45
22 - 26
-2 - +2
>80
ABG Result
pH
PCO2
HCO3BE
PO2
7.25
90
38
+12
34
Acute ventilatory failure superimposed on chronic
hypercapnia (chronic ventilatory failure) with severe
hypoxemia.
Pulse Oximetry

Pulse oximetry (SpO2) is the
noninvasive estimation of SaO2
Pulse Oximetry

SaO2
Pulse Oximetry

SaO2
Pulse Oximetry

SaO2
Pulse Oximetry

SaO2
Pulse Oximetry

Pulse oximetry may be used in any setting in
which a noninvasive measure of oxygenation
status is sufficient.




O2 therapy
Surgery
Ventilator management
Diagnostic procedures
 Bronchoscopy
 Sleep studies
 Stress testing
 Pulmonary Rehabilitation
Pulse Oximetry

Pulse oximetry uses light to work out oxygen
saturation. Light is emitted from light sources
which goes across the pulse oximeter probe
and reaches the light detector.
Pulse Oximetry

If a finger is placed in between the light source
and the light detector, the light will now have to
pass through the finger to reach the detector.
Part of the light will be absorbed by the finger
and the part not absorbed reaches the light
detector.
Pulse Oximetry

Hemoglobin (Hb) absorbs light. The amount of
light absorbed is proportional to the
concentration of Hb in the blood vessel. By
measuring how much light reaches the light
detector, the pulse oximeter knows how much
light has been absorbed. The more Hb in the
finger , the more light is absorbed.
Pulse Oximetry
Pulse Oximetry

The pulse oximeter uses two lights to analyze
hemoglobin, red and infared, to detect the
amount of oxyhemoglobin (O2Hb) and
deoxyhemoglobin (rHb)
Pulse Oximetry

The pulse oximeter works out the oxygen
saturation by comparing how much red light
and infra red light is absorbed by the blood.
Depending on the amounts of oxy Hb and
deoxy Hb present, the ratio of the amount of
red light absorbed compared to the amount of
infrared light absorbed changes.
Pulse Oximetry
Pulse Oximetry
Pulse Oximetry

Using this ratio, the pulse oximeter can then
work out the oxygen saturation.
Pulse Oximetry

Using this ratio, the pulse oximeter can then
work out the oxygen saturation.
Pulse Oximetry

Pulse oximeters often show the pulsatile change
in absorbance in a graphical form. This is called
the "plethysmographic trace " or more
conveniently, as "pleth".
Pulse Oximetry

If the quality of the pulsatile signal is poor,
then the calculation of the oxygen saturation
may be wrong. Always look at pleth before
looking at oxygen saturation.
Pulse Oximetry

Never look only at oxygen saturation !
Pulse Oximetry

Always look at pleth before looking at
oxygen saturation!
Pulse Oximetry

Interfering Substances




COHb
MetHb
Intravascular dyes (indocyanine green)
Nail polish or coverings
Pulse Oximetry

Interfering Factors






Motion artifact, shivering
Bright ambient lighting
Hypotension, low perfusion (sensor
site)
Hypothermia
Vasoconstriction drugs
Dark skin pigmentation
Pulse Oximetry

Criteria for Acceptability

Correlation with measured SaO2


SpO2 and SaO2 should be within 2% from
85-100%
Elevated levels of COHB (>3%) or MetHb
(>5%) may invalidate SpO2
Pulse Oximetry

Criteria for Acceptability

Adequate profusion of the sensor site
as seen in the plethysmographic
tracing and correlation with patient’s
heart rate
Pulse Oximetry

Criteria for Acceptability


Know interfering substances or agents
should be eliminated, e.g., nail
polishes, acrylic nails, etc.
Readings should be consistent with the
patient’s clinical history and
presentation.
Oxygen Saturation
Oxygen saturation is the ratio of either
oxygenated Hb (Oxyhemoglobin or O2Hb) to
total available Hb (reduced Hb or rHb + O2Hb)
or total Hb (O2Hb + rHb + COHb + MetHb),
depending on the instrumentation used to
measure and report values
Oxygen Saturation
Co – oximeters actually measures SaO2 using
spectrophotometry;
Ratio of oxyhemoglobin to total Hb:
SaO2 =
___
O2Hb
X 100
(O2Hb + rHb + COHb + MetHb)
Pulse oximeters estimate the SaO2 by using a noninvasive
probe that measures absorption or red and near-infrared
light;
Ratio of oxyhemoglobin to available Hb:
SpO2 =
O2Hb__ X 100
(O2Hb + rHb)
Oxygen Saturation
Oxyhemoglobin
(O2Hb)
1 2
3
Pulse
Oximeter
COOximeter
4
5
6
7
Reduced Hb
(rHb)
8
9
10
COHb + MetHb
11 12 13
O2Hb
O2Hb + rHb
O2Hb
O2Hb + rHb + COHb + MetHb
14
10
13
76%
SpO2
10
14
71%
SaO2
Oxygen Saturation
SaO2 is calculated by some blood gas analyzers
based on PaO2 and PH

Convenient but inaccurate!
SvO2 can be measured by a reflective
spectrophotometer in the pulmonary artery catheter
(Swanz-Ganz)
Oxygen Saturation
Normal Values
SaO2
= 97%
SvO2
= 75%
COHb
= .5% - 2% of Total Hb
MetHb
= 1.5% of Total Hb
Total Hb
= 14 – 16 gm% (males)
13 – 15 gm% (females)
Capnography
Capnography is the continuous,
noninvasive monitoring or expired CO2 and
analysis of the single-breath CO2 waveform
Capnography

Capnography


Allows trending of changes in alveolar and
dead space ventilation
End-tidal PCO2 (PetCO2) is reported in mm
Hg
Capnography
Normal Arterial & ETCO2 Values
ETCO2
Arterial CO2 (PaCO2)
from Capnograph
ETCO 2
RR
Normal PaCO2 Values:
Normal ETCO2 Values:
35 - 45 mmHg
30 - 43 mmHg
Capnography

Arterial - End Tidal CO2 Gradient
• In healthy lungs the normal PaCO2 to
ETCO2 gradient is 2-5 mmHg
• In diseased lungs, the gradient will
increase due to ventilation/perfusion
mismatch
Capnography
.


Normal
(ventilation) is 4 L of air per minute

Normal
(perfusion) is 5L of blood per minute.



So Normal
ratio is 4/5 or 0.8
When the
is higher than 0.8, it means
ventilation exceeds perfusion
When the
is < 0.8, there is a
mismatch caused by poor ventilation.
Capnography
Ventilation-Perfusion Relationships
Relationship between ventilated alveoli and
blood flow in the pulmonary capillaries
CO2 O2
Shunt perfusion
Alveoli perfused
but not ventilated
Normal
Ventilation and
perfusion is matched
Deadspace Ventilation
Alveoli ventilated but
not perfused
Capnography
..
Normal V/Q
ETCO2 - PaCO2
Gradient = 2 to 5 mmHg
CO2 O2
Capnography
..
•Mucus plugging
• ET tube in
right or left
main stem
bronchus
• Atelectasis
• Pneumonia
• Pulmonary
edema
Shunt Perfusion – Low V/Q
ETCO2 - PaCO2
Gradient = 4 to 10 mmHg
In short anything that
causes the alveoli to
collapse or alveolar filling
No exchange of O2 or CO2
Capnography
Dead Space Ventilation
. .
ETCO2 - PaCO2
Gradient is large
High V/Q
Ventilation is
not the problem!
Perfusion is the problem
No exchange of O2 or CO2occurs
Capnography
Dead Space Ventilation
ETCO2 = 33 mmHg
PaCO2 = 53 mmHg
53
53
0
0
0
53
0
Alveoli that do not
take part in gas
exchange will still
have no CO2 –
Therefore they will
dilute the CO2 from the
alveoli that were
perfused
0
0
0
The result is a widened ETCO2 to PaCO2 Gradient
Capnography
 Dead Space Ventilation

Disease processes that may cause Dead
Space Ventilation




Pulmonary embolism
Hypovolemia
Cardiac arrest
Shock
In short, anything that causes a significant
drop in pulmonary blood flow
Normal Capnogram - Phase I
CO2 mmHg
50
25
0
A
B
Beginning of expiration =
anatomical deadspace with
no measurable CO2
Anatomical Dead Space
Anatomical Deadspace
Conducting Airway - No Gas Exchange
 Anatomical Dead Space
 Internal volume of the
upper airways
•
•
•
•
Nose
Pharynx
Trachea
Bronchi
Normal Capnogram - Phase II
CO2 mmHg
50
C
25
0
B
Mixed CO2, rapid rise in
CO2 concentration
Normal Capnogram - Phase III
CO2 mmHg
50
Alveolar Plateau, all exhaled
gas took part in gas exchange
D
C
End Tidal
CO2 value
25
0
Time
Normal Capnogram - Phase IV
CO2 mmHg
50
Inspiration starts,
CO2 drops off rapidly
D
25
0
E
Capnography
Normal Capnogram
CO2 (mmHg)
50
37
0
Stable trend
Real-Time
Trend
Capnography
Hyperventilation - Decrease in ETCO2
CO2 (mmHg)
50
Real-Time
37
0
Possible Causes:
•
•
•
•
Increase in respiratory rate
Increase in tidal volume
Decrease in metabolic rate
Fall in body temperature
Trend
Capnography
Hypoventilation - Increase in ETCO2
CO2 (mmHg)
50
Real-Time
37
0
Possible Causes:
•
•
•
•
Decrease in respiratory rate
Decrease in tidal volume
Increase in metabolic rate
Rapid rise in body temperature
Trend
Capnography
Rebreathing
CO2 (mmHg)
50
Real-Time
Trend
37
0
Possible Causes:
• Expiratory filter that is saturated or clogged, expiratory valve
that is sticking
• Inadequate inspiratory flow, or insufficient
expiratory time
• Anything that causes resistance to expired flow
Capnography
Endotracheal Tube in Esophagus
CO2 (mmHg)
50
Real-Time
Trend
37
0
Possible Causes:
•
Missed Intubation - when the ET tube is in the esophagus, little
or no CO2 is present
NOTE: A normal capnogram is the best evidence that the ET
tube correctly positioned.
Case Study


A 29 year old male with head injury, and a
compound fracture of his femur sustained in a
motorcycle accident
2 weeks post trauma on mechanical ventilation
with the following physiological values:
PaCO2 – 42 mmHg
PaO2 – 95 mmHg
ETCO2 – 38 mmHg
Total Rate – 14 bpm
Minute Ventilation – 7 L/Min
Case Study
CO2 (mmHg)
50
Real-Time
37
0
Normal capnogram, stable trend
ETCO2/PaCO2 gradient 4 mmHg
Trend
Case Study
CO2 (mmHg)
50
Real-Time
Trend
37
0
Sudden decrease in ETCO2 from 38 mmHg to 18 mmHg
and remains there
RR – increases to 24 bpm
Minute Volume increases to 12 Lpm
Case Study
CO2 (mmHg)
50
Real-Time
37
0
ABG was drawn with the following results:
PaCO2
PaO2
PaCO2/ETCO2 gradient
38 mmHg
59 mmHg
20 mmHg
Trend
Case Study

Ventilation /perfusion lung scan was
consistent with a pulmonary embolism

A sudden drop in ETCO2, associated with a large
increase in the PaCO2/ETCO2 gradient, is often
associated with pulmonary embolism
Blood Gases and Related Tests
Questions?