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CAPNOGRAPHY
      presented by:
  Fred Halazon, NREMT-P
   Mike Burke, NREMT-P
     Cunningham Fire
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
Overview
History
Anatomy & Physiology
Capnographic waveform
Diagnosing different waveforms
Case studies
Relevance

ETT Verification
Cardiac Arrest
Ventilation
Bronchospastic Disease
Early detection of cellular hypoxia
History of capnography
Used by
anesthesiologists
since the 1970s

Standard of care in
the OR since 1991
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
History of Capnography in EMS


Pulse oximetry preceded capnography
Pulse oximetry measures oxygenation
Capnography measures ventilation
New technologies now allow use in EMS
Capnometry

Provides only a numerical measurement
of carbon dioxide (EtCO2)
Capnogram

A waveform display of carbon
dioxide over time
Definition of Capnography

Numerical value of the EtCO2 AND
Waveform of the concentration present in
the airway
Respiratory rate detected from the actual
airflow
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
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
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
Carbon Dioxide Transport

CO2 + H2O          H2CO3


Carbonic acid dissociates:

               +         _
H2CO3        H + HCO3
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%)
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
Physiology of CO2

Transported to the lungs in the blood
stream

Diffused across cell membrane into
alveoli

Eliminated during exhalation
Oxygen> lungs> alveoli> blood
                                           O2
 breath


CO2

  lungs                               Muscles + organs


CO2                                              O2

  blood

                          energy            cells




                                                Oxygen +
                    CO2                         Glucose
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
Capnographic Waveform


                  C                D



  A           B                         E
Inspiration           Expiration       Inspiration
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
0


    36

         40

              44
Physiology of CO2

Concentration of CO2 in alveoli is
determined by:


         PERFUSION (Q)

        VENTILATION (V)
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
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
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
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
Distinguishing between
oxygenation and ventilation
Normal Ventilation/Perfusion Ratio

The volume of blood returning to the
lungs matches the capacity of the lungs
to exchange gases

Ventilation
Cardiac Output
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
•If ventilation is held constant,
    then changes in EtCO2 are
    due to changes in cardiac
               output
Cardiac Output   EtCO2 (mm Hg)
      (L)
       2              20

      3               28

      4               32

      5               36
Break
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
Capnographic Waveform
     Height shows amount of CO2
     Length depicts time


45


0
Phases of Capnogram
     Expiratory segment

Consists of the following three phases
Phase I

Phase I- Represents CO2 free gas from
airways (Dead Space)
Phase I

    Beginning of exhalation



A    B




     I
Phase II

Phase II- Consists of rapid upswing (due
to mixing of dead space gas with alveolar
gas (Ascending Phase)
Phase II


Ascending Phase
                       C




         A
             B


                  II
Phase III

Phase III- Consists of an alveolar
plateau, CO2 rich gas, positive slope, rise
in PCO2 (Alveolar Plateau)
Phase III

                       Alveolar Plateau
        C          D



A   B




             III
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
Expiratory segment cont…
Alpha angle- Angle between phase II and
phase III (V/Q status of lung)

             C         D



    A   B                  E
Phases of Capnogram
     Inspiratory segment
Beta Angle- Angle between phase III and
descending limb of inspiratory segment

              C        D



     A   B                 E
Inspiratory segment

Phase 0- Inspiration, fresh gases inhaled
and CO2 falls rapidly to zero (Descending
Phase)
Phase 0


        C       D           Descending Phase
                            Inhalation
A   B                   E




                    0
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
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
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
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
Benefits in Hospital
Verification of ETT placement and
continuous monitoring
Cardiac Arrest
Ventilation
Procedural sedation
ETT Displacement


        Most likely occurs
         when patient is
             moved
Dislodged
Dislodged
Right Main Bronchi
CPR
Force, depth, and rate of chest
compressions

45




 0




     100% mortality if unable to achieve an EtCO2
           of 10 mm Hg after 20 minutes
CPR
ROSC
ROSC



45



 0
ROSC with NaHCO3
CPR
Positive pressure ventilation
Increased intrathoracic pressure
Pressure on Vena Cava, decreased
preload
Increased RR does not allow for
exhalation
CPR
Increased intrathoracic pressure leads to

Decrease in cardiac output, coronary
artery perfusion, and CPP
Optimize Ventilation
Titrate carbon dioxide levels in patients
sensitive to fluctuations
  Head Injuries
  Stroke
  Brain tumors
  Brain infections
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
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
Hyperventilation


45


0
Hypoventilation
Hypercapnia > 45 mmHg
How would hypoventilation change the
waveform? (4-12)
  Frequency
  Duration
  Height
  Shape
Hypoventilation



45


0
Bronchospasm
Alveoli unevenly ventilated on inspiration
Asynchronous emptying during
expiration
Alters Phase II—
  “Shark Fin” shaped waveform
Bronchospasm



45


0




 Bronchospasm
Bronchospasm
COPD
Asthma
       Initial




After therapy
Pneumothorax
Pulmonary Embolism
Hypercapnia/ RR~?
15 Sec Triage Tool
Rapidly assess pt
Toxins, chemical agents
Spontaneous
respirations
Patent airway with
adequate ventilation and
perfusion
Most acute pts
Seizures
15 Sec Triage Tool
       Terrorism (BNICE)
       Absorption skin and
       respiratory tract
       Respiratory
       depression
       Trends
Unresponsive patients
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
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
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
6 year old
 No recent medical hx or illnesses
 NKDA
 Clonidine for sleep aid at night
 Capnographic waveform
EtCO2: 50
  RR: 36
Decreased Cardiac Output
 94 y.o. Female
 DNR
 Respiratory distress
 Skin- ashen, cool, dry
HR: 31
EtCO2: 8
RR: 7
Case
 35 y.o. male
 DK, combative
 Possible OD
EtCO2: 34
 RR: 33
Documentation
Continuous waveform allows for legal
documentation
Proof of correct tube placement, RR,
EtCO2
Effectiveness of treatment in patient
care, early detection of deterioration
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.
Break Time
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.
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
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.
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.
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.
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.
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.
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.
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.
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.
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.
•   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.

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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
  • 3.
  • 4. Overview History Anatomy & Physiology Capnographic waveform Diagnosing different waveforms Case studies
  • 5. Relevance ETT Verification Cardiac Arrest Ventilation Bronchospastic Disease Early detection of cellular hypoxia
  • 6. History of capnography Used by anesthesiologists since the 1970s Standard of care in the OR since 1991
  • 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
  • 9. Capnometry Provides only a numerical measurement of carbon dioxide (EtCO2)
  • 10. Capnogram A waveform display of carbon dioxide over time
  • 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
  • 15. Carbon Dioxide Transport CO2 + H2O H2CO3 Carbonic acid dissociates: + _ H2CO3 H + HCO3
  • 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
  • 22. Capnographic Waveform C D A B E Inspiration Expiration Inspiration
  • 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
  • 24. 0 36 40 44
  • 25. Physiology of CO2 Concentration of CO2 in alveoli is determined by: PERFUSION (Q) VENTILATION (V)
  • 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
  • 34. Cardiac Output EtCO2 (mm Hg) (L) 2 20 3 28 4 32 5 36
  • 35.
  • 36. Break
  • 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
  • 38. Capnographic Waveform Height shows amount of CO2 Length depicts time 45 0
  • 39. Phases of Capnogram Expiratory segment Consists of the following three phases
  • 40. Phase I Phase I- Represents CO2 free gas from airways (Dead Space)
  • 41. Phase I Beginning of exhalation A B I
  • 42. Phase II Phase II- Consists of rapid upswing (due to mixing of dead space gas with alveolar gas (Ascending Phase)
  • 44. Phase III Phase III- Consists of an alveolar plateau, CO2 rich gas, positive slope, rise in PCO2 (Alveolar Plateau)
  • 45. Phase III Alveolar Plateau C D A B III
  • 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
  • 47. Expiratory segment cont… Alpha angle- Angle between phase II and phase III (V/Q status of lung) C D A B E
  • 48. Phases of Capnogram Inspiratory segment Beta Angle- Angle between phase III and descending limb of inspiratory segment C D A B E
  • 49. Inspiratory segment Phase 0- Inspiration, fresh gases inhaled and CO2 falls rapidly to zero (Descending Phase)
  • 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
  • 55. Benefits in Hospital Verification of ETT placement and continuous monitoring Cardiac Arrest Ventilation Procedural sedation
  • 56. ETT Displacement Most likely occurs when patient is moved
  • 60. CPR Force, depth, and rate of chest compressions 45 0 100% mortality if unable to achieve an EtCO2 of 10 mm Hg after 20 minutes
  • 61. CPR
  • 62. ROSC
  • 65. CPR Positive pressure ventilation Increased intrathoracic pressure Pressure on Vena Cava, decreased preload Increased RR does not allow for exhalation
  • 66. CPR Increased intrathoracic pressure leads to Decrease in cardiac output, coronary artery perfusion, and CPP
  • 67.
  • 68. Optimize Ventilation Titrate carbon dioxide levels in patients sensitive to fluctuations Head Injuries Stroke Brain tumors Brain infections
  • 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
  • 73. Hypoventilation Hypercapnia > 45 mmHg How would hypoventilation change the waveform? (4-12) Frequency Duration Height Shape
  • 75. Bronchospasm Alveoli unevenly ventilated on inspiration Asynchronous emptying during expiration Alters Phase II— “Shark Fin” shaped waveform
  • 78. COPD
  • 79. Asthma Initial After therapy
  • 83. 15 Sec Triage Tool Rapidly assess pt Toxins, chemical agents Spontaneous respirations Patent airway with adequate ventilation and perfusion Most acute pts Seizures
  • 84. 15 Sec Triage Tool Terrorism (BNICE) Absorption skin and respiratory tract Respiratory depression Trends
  • 85.
  • 86.
  • 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
  • 92. EtCO2: 50 RR: 36
  • 93. Decreased Cardiac Output 94 y.o. Female DNR Respiratory distress Skin- ashen, cool, dry
  • 95. Case 35 y.o. male DK, combative Possible OD
  • 97.
  • 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

  1. 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
  2. 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
  3. 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
  4. 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.
  5. 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.
  6. Beta angle increases with rebreathing
  7. 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)
  8. Stop compressions for 20 seconds decreased survival by 50%.
  9. 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.
  10. Hypercapnia causes cerebral vasodilation, which causes increased CBF, and further elevates ICP. Hypocapnia causes cerebral vasoconstriction, reduce ICP. Resulting in hypoperfusion. MAP-ICP=CPP