1. Capnography By
Lafe Bush

2. OBJECTIVES Define Review the respiratory cycle
Capnography, ETCO2, Capnometry
Review the respiratory cycle
Discuss waveform interpretation
Discuss disease specific waveform presentation

3. Terminology review
ETCO2 – Partial pressure of Carbon Dioxide at the end of an exhaled breath
PACO2 - Partial pressure of CO2 in the alveoli
PaCO2 - Partial pressure of CO2 in arterial blood
PETCO2 – Partial pressure of CO2 at the end of expiration
(a-ET)PCO2 – Arterial to end-tidal CO2 tension/pressure difference or gradient
PvCO2 – Partial pressure of CO2 in mixed venous blood
V/Q ratio – Ventilation to Perfusion ratio
PACO2: Partial pressure of CO2 in the alveoli (average of all CO2 in alveoli) PaCO2: Partial pressure of CO2 in arterial blood.
PETCO2: Partial pressure of CO2 at the end of expiration (correlates to ETCO2) (a-ET)PCO2: Arterial to end-tidal CO2 tension/pressure difference or gradient PvCO2: Partial pressure of CO2 in mixed venous blood

4. Terminology Review Cont.
Ventilation - moving air into and out of the lungs
Capnography - the continuous analysis and recording of Carbon Dioxide (CO2) concentrations in respiratory gasses (waveform and number)
Capnometry - the analysis of the gas with no waveform (number only)
Respiration - the process of providing oxygen to the body and removing CO2
Metabolism - the process of by which an organism obtains
energy
Aerobic = Glucose with oxygen
Anaerobic= Glucose without oxygen
Ventilation is normally a passive process however when receptors

5. Respiratory Cycle
Minute ventilation – total volume of gas entering the lungs per minute
Tidal Volume (Vt) volume of gas moved in one breath
(approx. 5-7 ML/KG (500 ML)
Dead Space (Vd) – volume of gas that does not reach the alveoli and does not participate in respiration (2ML/ KG (150LM)
Anatomical
Alveolar
Physiological
Alveolar Ventilation (Va) – volume of gas that reach the alveoli and participates in gas exchange (350 ML) (Vt – Vd = Va)
Anything that decreases the Vt only effects the Va not Vd
Anatomical dead space = trachea, bronchioles, and area not involved in gas exchange.
Physiological is due to a reason such as Atelectasis, injury, VQ mismatch.
Anatomical dead space cannot change so as Vt changes one must be remembering of the fact that dead space is the same.

6. Respiratory cycle
We initiate a breath when exhalation is complete and the pressure in the chest has become equal with the atmospheric pressure. Sensors in the respiratory center of the brain send messages via the phrenic nerve to the diaphragm to initiate another breath. As we take the next breath oxygen enters into the respiratory system and travels to the lungs and down to the alveoli. As the alveoli expand the alveolar membrane thins out (much like a balloon) allowing oxygen to diffuse into the red blood cells and carbon dioxide to diffuse into the lungs. This process occurs as a result of diffusion (gases in an area of higher concentration moving to an area of lower concentration) this is known as pulmonary respiration. The oxygen has now crossed into the pulmonary vein which then carries it to the left atrium then to the left ventricle where it is pumped out to the muscles and organs. The process for cellular respiration is similar to the process above where oxygen diffuses into the cell while carbon dioxide diffuses out of the cell mostly in the form of bicarbonate. The Co2 is then carried back to the lungs via the venous system and it is excreted.

7. Respiratory Cycle
In order for this previous process to work we must have three functioning components. We must have metabolism, perfusion, and ventilation.
Metabolism = which is the creation of energy using oxygen and glucose. Should something affect the body’s ability to produce energy or we would cease to exist.
Perfusion
Requires adequate blood volume including adequate red blood cells and hemoglobin's available to carry the oxygen
Intact pulmonary capillaries which are not blocked or damaged such as PE or pulmonary contusion
Efficient pump
Ventilation without ventilation there would be no intake of oxygen or elimination of CO2 which would eventually cause a destruction of all the prior processes and ultimately cause death.

8. PETCO2
In adults PETCO2 is lower than the PACO2 (average of all alveoli) by 2-5 mmHg
The difference between the two is the dead space
Reduction in cardiac output will result in decreased PETCO2 an increase in (a-ET)PCO2 and a decrease in ETCO2
Increased cardiac output will result in increased PETCO2
decreased alveolar dead space and a decreased (a-ET)
PCO2 and an increased ETCO2
Recently, using Fick's Principle, attempts were made to determine cardiac output non-invasively implementing periods of CO2rebreathing during which CO2 partial pressure of oxygenated mixed venous blood was obtained from the measured exponential rise of the PET value. In addition, oxygen uptake, carbon dioxide elimination, end-tidal PCO2, oxygen saturation, and tidal volume were determined. The results are encouraging in patients with healthy lungs.9 Whereas the results are controversial when the lungs are diseased.10
Under normal circumstances, the PETCO2 (the CO2 recorded at the end of the breath which represents PCO2 from alveoli which empty last) is lower than PaCO2 (average of all alveoli) by 2-5 mmHg, in adults.1-8 The (a-ET)PCO2 gradient is due to the V/Q mismatch in the lungs (alveolar dead space) as a result of temporal, spatial, and alveolar mixing defects. In healthy children, the (a-ET)PCO2gradient is smaller ( mm Hg) than in adults.9-14 This is due to a better V/Q matching, and hence a lower alveolar dead space in children than in the adults.9 The (a-ET)PCO2 / PaCO2 fraction is a measure of alveolar dead space, and changes in alveolar dead space correlate well with changes in (a-ET)PCO2.4 An increase in (a-ET)PCO2 suggests an increase in dead space ventilation. Hence (a-ET)PCO2 is an indirect estimate of V/Q mismatching of the lung.

9. ETCO2 Values 35-45mmHg normal > 45mmHg Hypoventilation
↓ RR = ↑ CO2
<35mmHg Hyperventilation
↑ RR or decreased perfusion = ↓CO2
Normal ETCO2 readings are equal to MMHG
When your respiratory rate decreases gas exchange decreases and ETCO2 increases.
When your respiratory rate increases gas exchange will increase and ETCO2 will decrease.
These are important factors to remember and can often be a hard thing to wrap your head around.

10. Normal Capnogram
At the end of inspiration, assuming that there is no rebreathing, the airway and the lungs are filled with CO2-free gases. Carbon dioxide diffuses into the alveoli and equilibrates with the end-alveolar capillary blood (PACO2 = PcCO2 = 40 mm Hg). The actual concentration of CO2 in the alveoli is determined by the extent of ventilation and perfusion into the alveoli (V/Q ratio). The alveoli with higher ventilation in relation to perfusion (high V/Q alveoli) have lower CO2 compared to alveoli with low V/Q ratio that would have higher CO2. As one moves proximally in the respiratory tract, the concentration of CO2 decreases gradually to zero at some point. The volume of CO2-free gas is termed respiratory dead space and here there is no exchange of oxygen (O2) and CO2 between the inspired gases and the blood. As the patient exhales, a CO2 sensor at the mouth will detect no CO2 as the initial gas sampled will be the CO2-free gas from the dead space. As exhalation continues, CO2 concentration rises gradually and reaches a peak as the CO2 rich gases from the alveoli make their way to the CO2 sensing point at the mouth. At the end of exhalation, the CO2concentration decreases to zero (base line) as the patient commences inhalation of CO2 free gases. 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.1 Any deviation from this identical shape should be investigated to determine a physiological or a pathological cause producing the abnormality.
Phase I = respiratory base line no carbon dioxide Represents the CO2-free gas from the airways (anatomical and apparatus dead space).
Phase II = the beginning of exhalation Consists of a rapid S-shaped upswing on the tracing (due to mixing of dead space gas with alveolar gas).where gas that was not involved in respiration is being eliminated (dead space).
Alpha angle is the transition from phase II to III and is an indirect indication of V/Q status of the lung
Phase III = Consists of an alveolar plateau representing CO2-rich gas from the alveoli. It almost always has a positive slope, indicating a rising PCO2 and is due to the following reasons:
Beta angle is transition from phase III to 0 The nearly 90 degrees angle between phase III and the descending limb in a time capnogram has been termed as the beta angle.5 This can be used to assess the extent of rebreathing.5 During rebreathing, there is an increase in beta angle from the normal 90 degrees. As rebreathing increases, the horizontal baseline of phase 0 and phase I can be elevated above normal.5,7-9 Occasionally, other factors, such as prolonged response time of the capnometer compared to respiratory cycle time of the patient, particularly in children, can produce increase in the beta angle with the elevation of the baseline of phase 0 and phase I, as observed in rebreathing.
 Any factors (such as cardiac output, CO2 production, airway resistance, functional residual capacity) that affects the V/Q ratio of the lung can influence the height and slope of phase III
Phase IIII or 0 = inspiration and is noted as a sudden down stroke as no ETCO2 is being exhaled.

11. INCREASED ETCO2 RESPIRATORY
Drug OD
Chocking (partial)
Respiratory failure
Air trapping disease
COPD
Asthma
<35 mild, tiring, > 50 tired (better do something)
Opiate which are central nervous system depressants. Come from opium poppy plant or a synthetic makeup. “opioid overdose triad”. The symptoms of the triad are:
pinpoint pupils
unconsciousness
respiratory depression.
Respiratory depression comes from the CNS involvement which controls our ability to breathe
Chocking
Where part of the respiratory tract is blocked ultimately decreasing the Vt and amount of air available for gas exchange.
Emphysema- decrease in alveolar membrane surface area so less gas exchange, more air then lung space causes problems with diffusion, and decrease to pulmonary blood flow. As the walls weaken the lungs cannot recoil and air is trapped.
Chronic Bronchitis –is the overproduction of mucus in the respiratory tract causing air trapping bellow.
Asthma
Initial trigger release of chemical mediators like histamine which causes the airways to swell. The second phase is the cells from the immune system attack the mucosa causing more swelling . Second phase is why we use steroids as it is usually not responsive to bronchodilators. This phase may start days or hours before the inflammation and may be noted on the waveform before the patient experiences severe SOB.

12. DECREASED ETCO2 RESPIRATORY
Hyperventilation (anxiety)
Can be used to train patient
Mucus Plug
Bronchospasm
Hyperventilation is due to an increased respiratory rate and the blowing of excessive CO2. Patients can be shown the waveform and corresponding respiratory rate which may give them something to concentrate on and help to lower respiratory rate.
Mucus plug can occur in patients with a trach or intubated patients and block gas exchange
Acute bronchospasm may not allow for gas exchange and can cause a decrease in ETCO2 (in extreme cases)

13. INCREASED ETCO2 METABOLISM
Pain
Increased heart rate = increased metabolism
Hyperthermia
Malignant hyperthermia will present with sharp increases in ETCO2
Shivering
Increased metabolism
Pain increases metabolism and thereby increases PETCO2 which correlates to an increase in CO2 elimination.

14. DECREASED ETCO2 METABOLIC
Diabetic Ketoacidosis (DKA)
ETCO2 <30 with a >BS = in children
Bradycardia
< ETCO2 due to decreased metabolism
Tachydysrhythmias
Seizures
<ETCO2 due to respiratory arrest

15. DECREASED ETCO2 PERFUSION
Severe Sepsis
Hypovolemic shock
Cardiogenic shock
Pulmonary embolism
Sepsis = Because of a decrease in the release of serum bicarbonate HCO3 the less acid is converted and brought to the lungs for elimination. This coupled with an increased respiratory rate causes a decrease in ETCO2.
Pulmonary embolism will cause an increase in dead space and thereby reduce ETCO2.

16. LIMITATIONS OF ETCO2
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

17. Pulse Oximetry Oxygen Saturation
O2 content/o2 capacity x 100
SPO2 changes lag up to several minutes in patients hypoventilating or apneic
Temperature sensitive
Hemodynamic sensitive
Oxygen combines with hemoglobin and is measured as oxygen saturation. Hemoglobin carries approximately 97% of the oxygen the remainder is carried in the plasma.
Pulse oximetry measures what is going out to the body ETCO2 measures what is coming back.

18. WAVEFORM INTERPITATION
Is there a waveform?
Is baseline flat or moving upward?
Expiratory upstroke?
Alveolar plateau?
Inspiratory downstroke?
Five things you need to have
height
frequency
rhythm
baseline
shape

19. FLAT WAVEFORM Capnograhy equipment not connected
Cardiac arrest/respiratory arrest
Missed intubation / Extubation
Ventilator disconnection
Remember the old days of the monitor going flat and making sure your patient was still connected before starting CPR
Make sure your patient did not go into respiratory or cardiac arrest
Make sure your ETT was not moved
For transports make sure the ventilator did not come disconnected.

20. EXPIRATORY UPSTROKE Air trapping disease = Prolonged or sloped
Alpha angle > 90° should make you consider a V/Q mismatch
Increased ETCO2 = Rise in upstroke
Relief of air trapping
Co2 delivery can be delayed for reasons such as COPD where the air is trapped in the lower airway causing the air to be released slowly and unevenly. The air that is exhaled last will have higher concentrations of CO2 in it which can be seen in the plateau phase.
Rise in ETCO2 will cause a rise in the height of the upstroke
ROSC, pacing capture, better ventilations
Relief of air trapping will cause the upstroke to be straighter

21. ALVEOLAR PLATEAU Air trapping = Rising plateau
Curare cleft = small dip
Pneumothorax = Decreasing plateau
Right mainstem intubation = biphasic waveform
ETT cuff leaking = Downward slopping plateau

22. WHAT CAN WE LEARN FROM ETCO2
Asthma, COPD, Anaphylaxis vs. CHF
Hypoventilation due to various medical reasons
Shock
Hyperventilation syndrome
Differentiation between air trapping diseases / Pneumonia / CHF
Effectiveness of treatments
Stable vs. unstable in patients with tachy/brady dysrhythmias
Ventilatory status of seizure patients
Progressing shock
Hyperventilation

23. INTUBATED PATIENTS Verification of ETT
ETT surveillance during transport and movement
Control of hypo/hyperventilation
CPR compression efficacy
Early signs of ROSC
Coming out of paralysis/sedation
ETT size/cuff inflation

24. TYPES OF DEVICES Semi – Quantitative capnometry Quantitative Waveform
Only tells you if there is ETCO2 or not. No number or waveform
Quantitative
Only gives a number no waveform
Waveform
Gives number and waveform
Semi – Quantitative = the old type applied to the end of the ETT and would change color Purple problem Yellow good.
 Purple -- EtCO2 < 0.5%
• Tan -- EtCO2 0.5-2%
• Yellow – EtCO2 >2%
Normal end-tidal CO2 is >4%; hence, the device should turn yellow when the endotracheal tube is inserted in patients with intact circulation.

25. SIDE STREAM VS. MAINSTREAM
Easy to connect
Can be used in awake patients
Patient position is not a factor
Can be used in conjunction with oxygen administration
Mainstream
No sampling tube (dead space)
No problem with water or other fluids in the sensor
No problem with pollutants entering the connector site
No delay in recording
Only utilized with ventilators

26. EQUIPMENT

27. Life Pack Monitor And ETCO2
Waveform disappears during charging
LP sweep speed 12.5 mm/sec print out 25mm/sec
M sweep speed 6.25 mm/sec
4 second screen shot
Shows CO2 for the last 20 seconds
ETCO2 must be > 3.5 to be displayed
RR is an average of the last 8 breaths
Because the monitor needs the energy when charging the waveform will become dashes. As soon as the shock is delivered the waveform will reset automatically within 20 seconds (LP)
Make sure to print out a strip as the waveform on the monitor will be compressed and could be different than actual. M = zoll m series
be careful with hypoventilating patients
watch for differences between # and waveform height

28. Normal Wave Form
Square box
ETCO

29. OBSTRUCTIVE AIRWAY Shark fin waveform
With or without prolonged expiratory phase
Can be seen before patient realizes symptoms
Indicative of asthma, COPD, or allergic reaction

30. INCREASED METABOLISM Acute change of > 10 – 15 mmHg
Decreased respiratory rate
Decreased VT
Increased Metabolic rate
Rise in body temp

31. Hyperventilation Shortened period between respirations
ETCO2 < 35 mmHg
CNS changes
Hyperventilation PE
VQ mismatch

32. LEAKING ETT CUFF Angled, sloping down stroke on the waveform
In adults can mean ruptured cuff or small ETT
Pediatrics indicates small ETT

33. WAKING UP TO SOON Curare Cleft is when paralysis wears off
Patient is taking a small breath that is causing the cleft
Re-paralyze

34. REVIEW What does A - B represent What does B - C represent
What does C - D represent
What does D - E represent
A – B = Represents the exhalation of dead space containing no CO2 proceeded by inspiration
B – C = Emptying of conducting ariway and beginning of alveoli emptying
C – D = Alveolar plateau gentle rise as etco2 is released
D - E = Inhalation

35. Question
ETT dislodgement
Respiratory Arrest

36. Question
Bronchospasm

37. Question
Rebreathing

38. QUESTION
Curare cleft

39. CASE STUDY
Pt awake and alert in exam room at Vanguard Medical. Presents w/ 3 week HX of bronchitis, and asthma. Finished oral steroids. Has been using inhaler. Denies fever, nausea, vomiting, diarrhea. Non productive cough with diffuse wheezing. Spo2 100% RA. Etco2 is 12. Carpal-pedal spasms present. Staff gave 1 albuterol Rx prior to ALS arrival. Pt calmed, and encouraged to breathe through her nose. Duo- neb d/c as we are unable to give w/o O2 and that was making her hyperventilation and finger spasms worse. ALS given per erp order, and PT transported w/o incident. Report to ern.

40. CASE STUDY

41. CASE STUDY
25yo male complaining of difficulty breathing. Patient has been using his inhaler for the past hour with no improvement. Patient states he has been intubated 1 time before, several years ago. Patient was in obvious distress speaking in 1-3 word sentences.
HR 120; BP 163/92; SPO2 94; RR 30; ETCO2 55

42. CASE STUDY Patient treated with albuterol/atrovent Epinephrine
Solu-Medrol
Magnesium
Ketamine and CPAP

43. Case Study 42 YO female found unresponsive in Walmart bathroom.
Grimaces to painful stimuli
RR 6
HR 96
BP 118/46
SPO
Blood Sugar 142
Pupils dilated
Lungs clear
What appear to be track marks to arms
ETCO2 41

44. Case Study

45. Case Study
Wife stated that the patient awoke today not feeling well, complaining of shortness of breath. The patient wife also stated that the patient was drooling which is new and had an unsteady gait while attempting to walk. Patient complained of pain in his left calf for the past two days. After getting up this morning, the patient ate breakfast and went back to bed. The patient slept most of the day and awoke about two hours ago. The patients breathing became worse and the wife called The patient has garbled speech but this was from a previous CVA. The patient denies chest pain, nausea, or vomiting. Skin cool, dry, lungs clear except for very slight expiratory wheeze right apex.
164/96
107 (sinus tachycardia)
Spo2 85% room air 90% 15 LPM via NRFM

46. CASE STUDY