Transcript Capnography: The Ventilation Vital Sign

CAPNOGRAPHY: THE
VENTILATION VITAL SIGN
Mazen Kherallah, MD FCCP
Critical Care Medicine and Infectious DIsease
Objectives
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Define Capnography
Discuss Respiratory Cycle
Discuss ways to collect ETCO2 information
Discuss Non-intubated vs. intubated patient uses
Discuss different waveforms and treatments of them.
So what is Capnograhy?
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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
Respiratory Cycle
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Breathing- Process of moving oxygen into the body
and CO2 out can be passive or non-passive.
Metabolism-Process by which an organism obtains
energy by reacting O2 with glucose to obtain
energy.
 Aerobic-
glucose+O2 = water vapor, carbon dioxide,
energy (2380 kJ)
 Anaerobic- glucose= alcohol, carbon dioxide, water
vapor, energy (118 kJ)
Respiratory Cycle con’t
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Ventilation- Rate that gases enters and leaves the
lungs
 Minute
ventilation- Total volume of gas entering lungs
per minute
 Alveolar Ventilation- Volume of gas that reaches the
alveoli
 Dead Space Ventilation- Volume of gas that does not
reach the respiratory portions ( 150 ml)
Respiratory Cycle
Oxygen -> lungs -> alveoli -> blood
Oxygen
breath
CO2
lungs
muscles + organs
Oxygen
CO2
energy
blood
CO2
cells
Oxygen
+
Glucose
Respiratory Cycle
ALL THREE ARE IMPORTANT!
METABOLISM
PERFUSION
VENTILATION
How is ETCO2 Measured?
Semi-quantitative capnometry
 Quantitative capnometry
 Wave-form capnography
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Semi-Quantitative Capnometry
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Relies on pH change
Paper changes color
 Purple
to Brown to Yellow
Quantitative Capnometry
Absorption of infra-red
light
 Gas source
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Side Stream
 In-Line
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Factors in choosing device:
 Warm up time
 Cost
 Portability
Waveform Capnometry
Adds continuous
waveform display to
the ETCO2 value.
 Additional
information in
waveform shape can
provide clues about
causes of poor
oxygenation.
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Interpretation of ETCO2
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Excellent correlation
between ETCO2 and
cardiac output when
cardiac output is low.
When cardiac output is
near normal, then ETCO2
correlates with minute
volume.
Only need to ventilate as
often as a “load” of CO2
molecules are delivered to
the lungs and exchanged
for 02 molecules
Hyperventilation Kills
EtCO2 Values
Normal 35 – 45 mmHg
 Hypoventilation > 45 mmHg
 Hyperventilation < 35 mmHg
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Physiology
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Relationship between CO2 and RR
 RR
 CO2
  RR   CO2
Hyperventilation
Hypoventilation
Why ETCO2 I Have my Pulse Ox?
Pulse Oximetry
Capnography
when patient is
hypoventilating or
apneic
Should be used with
Capnography
detected immediately
Should be used with
pulse Oximetry
Oxygen Saturation
Reflects Oxygenation
SpO2 changes lag
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Carbon Dioxide
Reflects Ventilation
Hypoventilation/Apnea
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What does it really do for me?
Non-Intubated Applications
Bronchospasms: Asthma,
COPD, Anaphlyaxis
Hypoventilation: Drugs,
Stroke, CHF, Post-Ictal
Shock & Circulatory
compromise
Hyperventilation
Syndrome: Biofeedback
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Intubated Applications
Verification of ETT
placement
ETT surveillance during
transport
Control ventilations during
CHI and increased ICP
CPR: compression efficacy,
early signs of ROSC,
survival predictor
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NORMAL CAPNOGRAM
NORMAL CAPNOGRAM
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Phase I is the beginning of exhalation
Phase I represents most of the anatomical dead space
Phase II is where the alveolar gas begins to mix with the
dead space gas and the CO2 begins to rapidly rise
The anatomic dead space can be calculated using
Phase I and II
Alveolar dead space can be calculated on the basis of :
VD = VDanat + VDalv
Significant increase in the alveolar dead space signifies
V/Q mismatch
NORMAL CAPNOGRAM
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Phase III corresponds to the elimination of CO2 from the
alveoli
Phase III usually has a slight increase in the slope as
“slow” alveoli empty
The “slow” alveoli have a lower V/Q ratio and
therefore have higher CO2 concentrations
In addition, diffusion of CO2 into the alveoli is greater
during expiration. More pronounced in infants
ET CO2 is measured at the maximal point of Phase III.
Phase IV is the inspirational phase
ABNORMALITIES
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Increased Phase III slope
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Obstructive lung disease
Sudden  in ETCO2 to
0
Dislodged tube
 Vent malfunction
 ET obstruction
Phase III dip
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Spontaneous resp
Horizontal Phase III with
large ET-art CO2
change
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Pulmonary embolism
  cardiac output
 Hypovolemia
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Sudden  in ETCO2
Partial obstruction
 Air leak
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Exponential 
Severe hyperventilation
 Cardiopulmonary event
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ABNORMALITIES
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Gradual 
Gradual increase
 Hyperventilation
 Fever
 Decreasing
 Hypoventilation
temp
 Gradual  in volume
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Sudden increase in
ETCO2
 Sodium
bicarb
administration
 Release of limb
tourniquet
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Increased baseline
 Rebreathing
 Exhausted
absorber
CO2
PaCO2-PetCO2 gradient
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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
LIMITATIONS
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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
USES
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Metabolic
 Assess
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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
PULMONARY USES
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Effectiveness of therapy in bronchospasm
Monitor PaCO2-PetCO2 gradient
 Worsening indicated by rising Phase III without plateau
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Find optimal PEEP by following the gradient. Should be
lowest at optimal PEEP.
Can predict successful extubation.
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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
Normal Wave Form
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Square box waveform
ETCO2 35-45 mm Hg
Management: Monitor
Patient
Dislodged ETT
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Loss of waveform
Loss of ETCO2 reading
Management: Replace
ETT
Esophageal Intubation
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Absence of waveform
Absence of ETCO2
Management: Re-Intubate
CPR
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Square box waveform
ETCO2 10-15 mm Hg (possibly higher) with
adequate CPR
Management: Change Rescuers if ETCO2 falls
below 10 mm Hg
Obstructive Airway
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Shark fin waveform
With or without prolonged expiratory phase
Can be seen before actual attack
Indicative of Bronchospasm( asthma, COPD, allergic
reaction)
ROSC (Return of Spontaneous
Circulation)
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During CPR sudden increase of ETCO2 above 1015 mm Hg
Management: Check for pulse
Rising Baseline
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Patient is re-breathing CO2
Management: Check equipment for adequate
oxygen flow
If patient is intubated allow more time to exhale
Hypoventilation
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Prolonged waveform
ETCO2 >45 mm Hg
Management: Assist ventilations or intubate as
needed
Hyperventilation
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Shortened waveform
ETCO2 < 35 mm Hg
Management: If conscious gives biofeedback. If
ventilating slow ventilations
Patient breathing around ETT
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Angled, sloping down stroke on the waveform
In adults may mean ruptured cuff or tube too small
In pediatrics tube too small
Management: Assess patient, Oxygenate, ventilate
and possible re-intubation
Curare cleft
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Curare Cleft is when a
neuromuscular blockade
wears off
The patient takes small
breaths that causes the
cleft
Management: Consider
neuromuscular blockade
re-administration
CAPNOGRAM #1
J Int Care Med, 12(1): 18-32, 1997
CAPNOGRAM #2
J Int Care Med, 12(1): 18-32, 1997
CAPNOGRAM #3
J Int Care Med, 12(1): 18-32, 1997
CAPNOGRAM #4
J Int Care Med, 12(1): 18-32, 1997
CAPNOGRAM #5
J Int Care Med, 12(1): 18-32, 1997
CAPNOGRAM #6
J Int Care Med, 12(1): 18-32, 1997
CAPNOGRAM #7
J Int Care Med, 12(1): 18-32, 1997
CAPNOGRAM #8
J Int Care Med, 12(1): 18-32, 1997
Now what does all this mean to me?
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ETCO2 is a great tool to help monitor the patients
breath to breath status.
Can help recognize airway obstructions before the
patient has signs of attacks
Helps you control the ETCO2 of head injuries
Can help to identify ROSC in cardiac arrest