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Capnography: Monitoring Ventilation and Detecting Tube Placement
1. CAPNOGRAPHY
presented by:
Fred Halazon, NREMT-P
Mike Burke, NREMT-P
Cunningham Fire
2. What is Capnography?
Noninvasive, continuous measurement of
exhaled carbon dioxide concentration over time
Digital display provides EtCO2 value
Provides a distinct waveform for each
respiratory cycle
7. History of Capnography in EMS
Colormetric- Useful device to confirm ET
tube placement in patients not in cardiac
arrest
Tube could be in esophagus or that
circulation is not bringing CO2 to the
lungs
Prone to contamination, leads to false
negatives
8. History of Capnography in EMS
Pulse oximetry preceded capnography
Pulse oximetry measures oxygenation
Capnography measures ventilation
New technologies now allow use in EMS
11. Definition of Capnography
Numerical value of the EtCO2 AND
Waveform of the concentration present in
the airway
Respiratory rate detected from the actual
airflow
12. Definitions
PACO2—Partial pressure of CO2 in the alveoli
PaCO2—Partial pressure of CO2 in arterial
blood
PEtCO2—Partial pressure at the end of
expiration
PvCO2—Partial pressure of CO2 in mixed
venous blood
PCO2—Partial pressure of CO2
13. Definitions
PaO2—Partial pressure of O2 in arterial blood
(hypoxemia)
SPO2—Saturation of arterial blood (POX)
percent
SaO2—Percentage of arterial hemoglobin
saturated with O2 (POX)
PO2—Partial pressure of O2
14. What is Carbon Dioxide?
Capnos comes from the Greek word for
“smoke”
Smoke from the Fire of metabolism
Natural waste product of cellular activity
CO2 is a compound molecule
2 elements of oxygen and 1 element of
carbon
Colorless and heavier than air
16. Gas Transport in Blood
O2 carried in blood
Dissolved in blood plasma
Bound to hemoglobin with iron
CO2 carried in blood
Dissolved in plasma (5-10%)
Chemically bound to hemoglobin in (RBC’s)
(carbaminohemoglobin) (20-30%)
Most carried as bicarbonate ions (HCO3-)
(60-70%)
17. Physiology of CO2
End of inspiratory cycle, airways filled
with CO2 free gas
CO2 is a product of cellular metabolism
CO2 is continuously diffused across the
cell membrane into the circulating blood
18. Physiology of CO2
Transported to the lungs in the blood
stream
Diffused across cell membrane into
alveoli
Eliminated during exhalation
19. Oxygen> lungs> alveoli> blood
O2
breath
CO2
lungs Muscles + organs
CO2 O2
blood
energy cells
Oxygen +
CO2 Glucose
20.
21. Physiology of CO2
The evolution of CO2 from the alveoli to
the mouth during exhalation, and
inhalation of CO2 free gases during
inspiration gives the characteristic shape
to the CO2 curve which is identical in
all humans with healthy lungs
23. Physiology of CO2
Alveoli in lower lung is more perfused,
but less ventilated
In the more proximal respiratory tract, the
CO2 falls gradually to zero at some point
26. Physiology of CO2
Concentration of CO2 in alveoli:
Varies INDIRECTLY with ventilation
Increase Ventilation: Decrease CO2 in Alveoli
Decrease Ventilation: Increase CO2 in Alveoli
Varies DIRECTLY with perfusion
Decrease Perfusion: Decrease CO2 in Alveoli
Increase Perfusion: Increase CO2 in Alveoli
27. Oxygenation and Ventilation
What is the difference?
Oxygenation: is the transport of O2 via
the bloodstream to the cells
Oxygen is required for metabolism
Ventilation: is the movement of air into
and out of the lungs
exhaling of CO2 via the respiratory tract
Carbon dioxide is a byproduct of metabolism
28. Oxygenation
Measured by pulse oximetry (SpO2)
Noninvasive measurement
Percentage of oxygen in red blood cells
Changes in ventilation take several minutes
to be detected
Affected by motion artifact, poor perfusion,
temperature
29. Ventilation
Measured by the end-tidal CO2
Partial pressure (mm Hg) or volume (%) of
CO2 in the airway at end of exhalation
Breath-to-breath measurement provides
information within seconds
Not affected by motion artifact, distal
circulation, temperature
31. Normal Ventilation/Perfusion Ratio
The volume of blood returning to the
lungs matches the capacity of the lungs
to exchange gases
Ventilation
Cardiac Output
32. Ventilation-Perfusion (V/Q)
Mismatch
Phenomenon where either perfusion or
ventilation to an area of lung decreases;
results in diminished gas exchange,
hypoxemia, and hypercapnia
33. •If ventilation is held constant,
then changes in EtCO2 are
due to changes in cardiac
output
37. Value of the Capnographic Waveform
Provides valid EtCO2 value
Visual assessment of patient airway
integrity
Verify proper ET tube placement (with
pulmonary perfusion)
Waveforms have characteristic shape
like an ECG
46. Slope of Phase III
CO2 is being continuously excreted into
the alveoli
Late emptying of alveoli with lower (V/Q)
ratios, produces higher PCO2
End-tidal
End of the wave of exhalation
50. Phase 0
C D Descending Phase
Inhalation
A B E
0
51. End-tidal CO2 (EtCO2)
Allows monitoring for changes in
Ventilation—Asthma, COPD, airway edema,
FBAO, stroke
Diffusion—Pulmonary edema, alveolar
damage, CO poisoning (COHb), smoke
inhalation, hydrogen cyanide
Perfusion—shock, pulmonary embolus,
cardiac arrest, severe dysrhythmias
52. Decreased EtCO2
Decreased Metabolism Respiratory System
Analgesia/ sedation Alveolar hyperventilation
Hypothermia Bronchospasm
Mucus plugging
Circulatory System Equipment
Cardiac arrest Leak in system
Embolism Partial obstruction
Sudden hypovolemia or ETT in hypopharynx
hypotension
53. Increased EtCO2
Increased Metabolism Respiratory System
Pain Respiratory insufficiency
Hyperthermia Respiratory depression
Malignant hyperthermia Obstructive lung disease
Shivering
Circulatory System Equipment
Increased cardiac output Defective exhalation valve
with constant ventilation Exhausted CO2 absorber
54. Major Benefits in Pre-Hospital
Verifying ETT placement and continuous
monitoring of position during transport
Cardiac Arrest
Effectiveness of cardiac compression
Predictor of survival
Ventilation
Bronchospastic Disease
69. Optimize Ventilation
Carbon dioxide affects cerebral blood
flow (CBF)
Influencing intracranial pressure
Hypercapnia causes vasodilation
Hyperoxygenate, NOT hyperventilate
Hyperventilation does not improve
oxygenation
Maintain CO2 of 35-40 mm Hg
70.
71. Hyperventilation
Hypocapnia < 35 mmHg
Normal range is 35-45 mm Hg (5% vol)
How would hyperventilation change the
waveform? (26-30)
Frequency
Duration
Height
Shape
88. 6 year old female
Status seizure
Found supine in bed with L disconjugate gaze
Unresponsive to stimuli
Vomiting
B/P- 136/66
HR- 136
RR- 40
Skin- warm, dry, acyanotic
89. 6 year old
Tx pt to pram controlling airway
Supplemental O2
Unable to establish IV
Administer 5mg Valium PR
B/P- 108/70
HR- 116
RR- 36
90. 6 year old
Heent- Clr
Perrla
Chest = rise/fall w/clr BS B/L
ABD= snt
Pelvis= stable
SmoeX4 w/o angulation
Back Clr
No visual signs of Trauma
91. 6 year old
No recent medical hx or illnesses
NKDA
Clonidine for sleep aid at night
Capnographic waveform
98. Documentation
Continuous waveform allows for legal
documentation
Proof of correct tube placement, RR,
EtCO2
Effectiveness of treatment in patient
care, early detection of deterioration
99. The era is over when we can justify not
knowing whether an ETT is in place or
not.
We may not be able to intubate
everybody, but we must always know
when the tube is in place or not.
101. What is up coming and how
Capnography will assist
The newest phase in CPR Protocols.
How it will effect our decisions to work a
patient or not.
The CPR first protocols.
Therapeutic Hypothermia.
102. What is Therapeutic
Hypothermia
Is an evidence based change in Cardiac
Arrest patients
This change effects treatment of the
patient with a return to spontaneous
pulses.
The studies show good stats that back
up this method of treating patients
103. The European Study
This study was conducted in Nine
hospitals and 5 countries.
The Study was performed completely
random.
The patients were accepted into the
study based on speed of response to V-
fib arrest.
104. The Australian study
Less involved study.
This study took place in Melbourne and
involved four hospitals
This study was done Pseudo random
format with patients selected based on
an odd or even day.
105. Criteria
The patient to be accepted into the study had
to be a persistent V-fib arrest and still in coma
state u/a to hospital.
The patient must have Resuscitation efforts
performed by trained personnel within 5-15
minutes of collapse.
The patient must also have ROSC in under
sixty minutes.
The patient must also be intubated and
ventilated.
106. European Study Procedures
The patient was cooled to 32 to 34
degrees Celsius.
This temp was reached in the first four
hours of the resuscitation.
Pt was held at this temp for twenty four
hours and then passively re-warmed.
107. Australian Study
Pt. Accepted on the same criteria
however it was based on if it was an odd
or even day.
The pt were cooled to 33 degrees
Celsius and kept there for 12 hours and
the actively re-warmed after 18 hours.
108. The Results and they were
impressive!
In the European Study 75 of 136
patients(55%) had a favorable
neurological outcome.
In the normothermic patients the results
were still good but not great at 39%
The Australian Study showed a 49%
save rate in the hypothermic pt and a
26% in the normothermic pt.
109. Why do this work?
The proof is in the pudding for its
benefits.
However the actions is slightly more
theoretical.
Fist is hypothermia lowers the cerebral
metabolic rate for oxygen by 6% for every 1
degree C
Second hypothermia suppresses chemical
reactions.
110. If this so great why don’t we
use it!
Simple Logistics
The patient once taken to the
hypothermic state must remain there to
have benefit. A Rolla coaster approach is
not going to work.
The equipment to do this efficiently and
controlled is expensive but is expected to
fall in price as it becomes more widely
spread.
111. References
• Barton, C. & Wang, E. (1994). Correlation of End-Tidal CO2
Measurements to Arterial PaCO2 in Nonintubated Patients. Annals
of Emergency Medicine, 23 (3): 561-562.
• Bergenholtz, K.F., RN, MSN, CRNP-CS. (2004). Using and
understanding Capnography. Microstream capnography solutions.
karen.bergenholtz@oridion.com.
• Bhavani-Shankar, K., MD, Philip, JH. Defining segments and phases
of a time capnogram. Anesthesiology Analg (2000). 91(4): 973-977.
• Bhavani-Shankar, K., MD. http://capnography.com/
• Falk, J.L., Rackow, E.C., Weil, M.H. End-tidal carbon dioxide
concentration during cardiopulmonary resuscitation. New England
Journal of Medicine (1998) 318(10): 607-611.
• Fowler, Ray, MD, FACEP. www.rayfowler.com
• Fowler, W.S. Lung Function studies, II. The respiratory deadspace.
American Journal of Physiology. (1998) 154: 405-416.
• Kanowitz, A., MD, FACEP, EMS Director, Arvada, CO. (2004).
[Capnography in EMS]. Unpublished raw data.
112. • Katz SH, Falk JL. Misplaced endotracheal tubes by paramedics
in an urban emergency medical services system. Annals of
Emergency Medicine (2001) 37(1): 32-37.
• Medtronic Physio-Control Corporation (2005).
http://www.healthcareeducation.org
9. Raff, Hershel, PhD, (2003). Physiology Secrets (2nd ed.)
Philadelphia, PA: Hanley & Belfus.
10.Scanlon, V.C. & Sanders, T., (1999). Essentials of Anatomy and
Physiology (3rd ed.) Philadelphia, PA: F.A. Davis Co.
11.Thompson, J.E., RRT, FAARC, Jaffe, M.B., PhD. (2005 Jan).
Capnography waveforms in the mechanically ventilated patient.
Respiratory Care. 50(1): 100-109.
12.Wik L, et al: “Quality of cardiopulmonary resuscitation during
out-of-hospital cardiac arrest.” JAMA. 293(3): 299-304, 2005.
13.Woodruff, D.W., RN, CNS, CCRN, MSN. (2006 Jan/Feb)
Deciphering Diagnostics. Nursing made incredibly easy!, 4(1):
4-10.
Editor's Notes
70% in patients in cardiac arrest– clogged, no CO2-O2 exchange taking place (cellular metabolism) 5%= 35-37 mmHg Yellow could by gastric acid, drugs
CO2 enters blood, most diffuses into red blood cells, which contain the enzyme CARBONIC ANHYDRASE. The enzyme catalyzes the reaction of carbon dioxide and water to form carbonic acid: Carbonic acid then dissociates. The Bicarbonate ions diffuse out of the red blood cells into the plasma, leaving HYDROGEN IONS (HEMOGLOBIN BUFFERS THE IONS, CL- (CHLORIDE IONS) enter the red blood cell When the blood reaches the lungs, an area of lower PCO2, these reactions are reversed, CO2 is re-formed and diffuses into the alveoli. Eliminated during exhalation
O2 carried by weak bond with hemoglobin (98.5%) each hemoglobin can bind FOUR molecules of O2 (HbO2) oxyhemoglobin 10%= dissolved in blood 20%= HbCO2= carbaminohemoglobin 70%= bicarbonate ions
Stroke volume- amount of blood ejected by the left ventricle with each contraction approximately 60-80ml. Varies with age, sex, health. Tidal volume- amount of air inspired and expired in a normal breath.
Low cardiac output caused by cardiogenic or hypovolemia resulting from hemorrhage wont carry as much co2 back to the lungs, resulting in lower co2. Doesn’t mean the pt is hyperventilating, or their arterial co2 level will be reduced. Reduced perfusion to the lungs alone causes this phenomenon. Lung function is perfectly normal.
Beta angle increases with rebreathing
Hydrogen cyanide byproduct of combustion, plastics in house fires. CO= Leading cause of death from fire. Hemoglobin’s affinity for CO is over 240 times greater than O2. CO forms CARBOXYHEMOGLOBIN (COHb)
Stop compressions for 20 seconds decreased survival by 50%.
A sudden rise in EtCO 2 indicates increased cardiac output. Cardiac output immediately after ROSC is often low and drugs such as epinephrine can produce peripheral vasoconstriction, so palpating a pulse may be very difficult. The presence of an organized rhythm on the monitor accompanied by a sudden increase in EtCO 2 indicates ROSC has occurred and cardiac output has improved despite questionable pulses.
Hypercapnia causes cerebral vasodilation, which causes increased CBF, and further elevates ICP. Hypocapnia causes cerebral vasoconstriction, reduce ICP. Resulting in hypoperfusion. MAP-ICP=CPP