1. Continuous Capnography ~ The “Wave” of the Future
Amy Gutman MD ~ EMS Medical Director

2. Objectives What is the capnogram?
Review capnogram appearance in relation to physiology with clinical implications
Incorporate capnography into protocols
The program was designed to meet the following learning objectives.
At the completion of this program you will be to:
Relate a normal capnogram to the phases of breathing
List five clinical applications for capnography
Identify the four most common abnormal capnograms
Describe how to incorporate capnogram to patient care according to your local protocol
Appreciation to Medtronics for 2010 permission to use portions of their training module in preparing this presentation

3. Waveform Capnography
Non-invasive, continuous measurement of airway CO2 concentration
“Vital” sign of patient’s ventilatory & hemodynamic status
Provides an early objective measurement & warning of changes in ventilation & cardiopulmonary status from one breath to another
Important for medico-legal documentation
Standard of care for prehospital & hospital patient monitoring

4. Carbon Dioxide (CO2) & End-Tidal CO2 (ETCO2)
“Capnos”
From the Greek: “smoke” & “fire of life” (metabolism)
Greeks were smart ~ CO2 produced as a waste product of metabolism
CO2 diffused into bloodstream, transported to lungs, perfused into alveoli, eliminated / exhaled through airway
ETCO2 is amount of CO2 measured at the peak of the exhalation wave
What is End-Tidal CO2?
Breaking the term apart, “carbon dioxide at the end of the tide”
Breathing is done in waves (in and out)
EtCO2 is the amount of CO2 measured at the peak of the wave going out at the end of exhalation
EtCO2 is measured at the nose, mouth, or hub of the ET tube

5. Prehospital Capnography
Used by anesthesiologists to monitor sedated patients since 1970s
For hospitals, in 2001 JCAHO recommended capnography as standard of care for all procedural sedation to monitor vital signs, oxygenation & ventilation
In 2010 the journal Cardiology published the new AHA Guidelines recommending capnography as standard of care in monitoring prehospital patients with respiratory distress, post-advanced airway management, & during / post-resuscitation
Capnography is not new.
The technology was initially used for monitoring anesthetized patients in the OR.
New technology is now available for EMS in both intubated and non-intubated patients.

6. AHA 2010 Guidelines Summary
Continuous waveform capnography recommended for intubated patients throughout arrest / peri-arrest period
Confirm ETT Placement (Class I, LOE A)
Continuous monitoring of patient, airway, equipment
Monitor CPR quality (Class IIb, LOE C)
<10mmHg not associated with successful resuscitation or effective compressions
Push Hard, Push Fast
Change rescuer every 2 minutes
Detect ROSC (Class IIa, LOE B)

7. Capnography Methods CALORIMETRY CAPNOMETRY
Litmus paper in which color changes indicate qualitative CO2 in exhaled air
Intubated patients only
Impaired by moisture / secretions
False (-) in arrest or shock states
Equates to “checking a pulse”
Continuous waveform of quantitative values for ETCO2 concentration in exhaled air
All patients
Equates to “monitoring ECG”
Colorimetric
This is basically a device that contains specially treated litmus paper, that changes color indicating the amount of CO2 detected. Litmus paper changes color in reaction to the an acid-base balance and carbon dioxide is a gaseous state of carbonic acid.
This disposable detector for intubated patients only; it fits on the hub of the ET tube.

8. Low Flow Capnography
High flow and mainstream options for hospitalized patients; side-stream is most common prehospital monitoring method
Sidestream:
All age groups, intubated & non-intubated
50cc air required for sampling
No calibration required
Disposable tubing / cannulas
Durable for EMS environment
Mainstream ETCO2 measurement is a more direct method of measuring exhaled CO2 in intubated patients

9. Documentation
Printed confirmation of procedural skills & patient responses to treatment
No further “blame games”, i.e. “The tube was in place until you dislodged it”
Prints out both waveform & patient trends
State requirement to attach the waveform summary to your PCR (similar to an EKG)
Documentation of this objective data on your patient includes: -

10. OXYGENTATION VENTILATION
O2 bloodstream to cells
Non-invasive measurement by pulse oximetry (SpO2) of %O2 in RBCs
Changes in ventilation take minutes to be detected
Affected by motion artifact, poor perfusion & some dysrhythmias
Exhaling of CO2 metabolism byproduct via respiratory tract
Measured by ETCO2 as a partial pressure (mmHg) or volume (% vol) of CO2 in airway at end of exhalation
Breath-to-breath measurement provides info within seconds
Not affected by motion artifact, poor perfusion or dysrhythmias
Two completely different and separate functions:
• Oxygenation is the transport of O2 via the bloodstream to the cells
- Oxygen is required for metabolism
• Ventilation is the exhaling of CO2 via the respiratory tract
- Carbon dioxide is a byproduct of metabolism
Capnogram from

11. INCREASED ETCO2 DECREASED ETCO2
METABOLISM
Pain
Hyperthermia
Shivering / Increased Muscle Activity
RESPIRATORY
Depression / Hypoventilation
COPD
Analgesia / Sedation
Effective Bronchospasm Treatment
CIRCULATORY
Increased cardiac output
Effective Compressions
MEDICATIONS
Sodium Bicarbonate
METABOLISM
Hypothermia
Metabolic Acidosis
Decreased muscular activity
RESPIRATORY
Hyperventilation
Bronchospasm
Mucus Plugging / Obstruction
CIRCULATORY
Decreased cardiac output
Shock states
Cardiac Arrest
Pulmonary Emboli

12. Capnography Waveform 1 waveform = 1 respiratory cycle
Height = amount of CO2
Length = time of respiratory cycle
Information in 4 second views; Printouts in “real-time” views
Baseline usually “0” as no CO2 normally present during inspiration
Normal range is 35-45mm Hg (5% vol)

13. Capnogram Phase I: Dead Space Ventilation
Beginning of exhalation when no CO2 present
Air from trachea, posterior pharynx, mouth & nose AKA “dead space” as no gas exchange occurs in these areas A B

14. Capnogram Phase II: Ascending Phase
“Early Exhalation Phase”
CO2 from alveoli reaches the upper airway & mixes with dead space air
Causes a rapid rise in CO2 levels which is detectable in exhaled air C B

15. Capnogram Phase III Alveolar Plateau
At this point, CO2 rich alveolar gas is majority of exhaled air
Uniform “plateau” CO2 concentration from alveoli to nose / mouth
Highest CO2 concentration (End-Tidal CO2) at end of tidal breath / alveolar plateau (“D”)
Normal ETCO2 = 35-45mmHg
In phase three, the carbon dioxide from the alveoli has reached the airway exit. The exhaled air is now rich in CO2. In normal ventilation of health lungs, the concentration of CO2 in the air is uniform. C D

16. Capnogram Phase IV: Descending Phase
Inhalation / Inspiration begins & O2 rapidly fills the airways
CO2 level quickly drops to “0” baseline E D

17. ETCO2 Monitoring Airway Breathing / Ventilation
Verification & continuous monitoring of ETT placement
Breathing / Ventilation
Movement of air in & out of the lungs in respiratory illnesses
Hyperventilation / Hypoventilation
Bronchospasm, Restrictive, Obstructive breathing pattern differentiation
Circulation / Perfusion
Monitor low perfusion states & circulation of oxygenated blood
Effectiveness of cardiac compressions & 1st indicator of ROSC
Shock, pulmonary embolus, cardiac arrest, prolonged arrhythmias
Diffusion
Gas exchange between air-filled alveoli & pulmonary circulation
Pulmonary edema, alveolar damage, CO poisoning, smoke inhalation
End-tidal CO2 reflects changes in:
• Ventilation - the movement of air in and out of the lungs
• Diffusion - the exchange of gases between the air-filled alveoli and the pulmonary circulation
• Perfusion - circulation of blood through the pulmonary capillaries

18. Clinical Capnography

19. Systematic Interpretation
“Is there CO2 present?”
If there is a waveform, there is CO2
If there is no waveform there is an issue with patient, airway or equipment.
“Does the ETCO2 value return to zero during inhalation / respiratory baseline?”
If waveform does not return to baseline then patient rebreathing exhaled CO2.
“Does waveform shape rise steeply, plateau, then steeply return to the baseline?”
Sloping, notching, or prolonged waveform are signs of abnormalities.
“What is the ETCO2 level?”
Normal=35-45 mmHg, >45mmHg=hypercapnia, <35mmHg=hypocapnia.

20. Intubated Patients (Non-Arrest)
Verify & continuously confirm ETT placement
Immediately detect ETT position changes
Optimize ventilation management

21. ETT Placement Confirmation*
Annals of EM 2005; 45:
No unrecognized misplaced endotracheal intubations were found in patients for whom paramedics used continuous ETCO2 monitoring.
Failure to use continuous ETCO2 monitoring associated with a 23% unrecognized misplaced intubation rate
Standard of care for confirmation & monitoring of the intubated patient is waveform capnography, pulse oximetry, & physical confirmation (i.e. auscultation, tube fog)
Presence of exhaled CO2 indicates tracheal placement within seconds of proper placement
Esophageal ETT placement may briefly detect CO2 but residuals “washed out” within 6 positive-pressure ventilations
Gastric CO2 from: carbonated beverages, Tums, gastric distention from mouth to mouth ventilation
These challenges are addressed by the American Heart Association in the International Guidelines 2000:
“… emergency responders must confirm tracheal tube position by using nonphysical examination techniques.” P I-87
Secondary confirmation with an EtCO2 or esophageal detection has a Class IIa recommendation. P I-150
Source: Guidelines 2000 for Cardiovascular Resuscitation and Emergency Cardiovascular Care, Circulation 102 (suppl I) 8. August 22,2000
*Guidelines 2000 for Cardiovascular Resuscitation & Emergency Cardiovascular Care, Circulation. August,2000

22. ETT Displacement 4 5
Traditional “physical” methods of monitoring ETT position subjective, unreliable & delayed
ETT displacement likely to occur when patient moved in & out of the transport vehicle & from the stretcher to bed
Useful “warning sign” when providers have other responsibilities
Sudden drop in ETCO2 immediately signals obstructed or dislodged tube
Detection of a displaced or obstructed ETT using pulse oximetry or changes in HR / BP can be delayed 2-3 minutes*
*Guidelines for Cardiovascular Resuscitation &Emergency Cardiovascular Care, Circulation August, 2000

23. How Good Is ETCO2 In the Intubated Patient ?
1999: 1st research demonstrating efficacy of ETCO2 in prehospital ETI: “Confirmation of Airway Placement” (Sayre, M. PEC)
108 patients intubated in the field
52 trauma, 56 medical patients
ETT placement at ED arrival showed 27 pts (25%) had improperly placed ETT
18 esophageal, 9 oropharyngeal
No patients with quantitative capnography had misplaced ETTs
Silvestri S. “Improvement in Misplaced ETT Recognition within a Regional EMS System” (AEM. 2003)
108 patients intubated in the field
9% had improperly placed ETT
No unrecognized misplaced ETT in pts with continuous ETCO2 monitoring

24. Cuff leak
It is not uncommon during to have a small cuff leak which may not be evident until many minutes / hours post intubation
Continuous waveform will begin to show “gaps” or a “slide off” dependent on the area / severity of the leak

25. Assess Effectiveness of Chest Compressions
With constant ventilation, non-invasive capnography correlates with the blood flow / circulatory status produced by compressions
Good correlation between ETCO2 & cardiac output
Low cardiac output reduces blood flow to the lungs & fails to clear CO2 from the bloodstream
Properly done chest compressions provide
25-30% of normal blood supply to the brain
5%-10% of normal blood supply to the heart
Adequate chest compressions promote the elimination of metabolic wastes
A spike in ETCO2 indicates ROSC prior to any other “vital” sign
Airway- open with ET tube - confirmed with EtCO2.
Breathing - controlled and stable - monitored by capnography.
Circulation - cardiac output directly related to changes in EtCO2.
Capnography provides a non-invasive method for monitoring blood flow generated by CPR.

26. Rescuer Fatigue & Compressions4 5
Ochoa Study
Rescuers not able to maintain adequate compressions for >1 minute
Rescuers did not perceive fatigue even when measurably present
Increased ETCO2 correlates with:
Fresh rescuer with same or faster compression rate
Mechanical compressions
Use ETCO2 feedback to modify compression depth / rate / force

27. Detecting ROSC 4 5
Continuous ETCO2 an almost immediate indicator of successful resuscitation
Sudden increase in ETCO2 is an indicator that cellular metabolism has resumed & that pulses soon to be regained (cardiac output increasing)
Arrhythmia / arterial vasoconstriction makes pulses initially difficult to detect
After 2 mins, briefly stop CPR & check for organized rhythm on ECG monitor
Capnography predicts probability of successful outcome following resuscitation & may be used in the decision to cease resuscitation efforts
ETCO2 <10 mmHg throughout the duration of a code signals a poor outcome.

28. ETCO2 90% sensitive in predicting ROSC
Canitneau J. ETCO2 during CPR in humans presenting mostly with asystole. Critical Care Medicine. 1996
Wayne M. Use of ETCO2 to Predict Outcome in Prehospital Cardiac Arrest. Annals of EM. 1995
120 non-OOHCA patients
ETCO2 90% sensitive in predicting ROSC
Maximal ETCO2 <10mmHg during 1st 20 minutes after intubation never associated with ROSC (0%)
90 medical OOHCA PEA patients
100% mortality if unable to achieve ETCO2 >10mmHg after 20 minutes
16 survivors
In 13 survivors a rapid rise of ETCO2 was earliest ROSC indicator
1-3 mins before palpable pulse
3-7 mins prior blood pressure

29. Return of Respiratory Drive
If a “previously dead” or RSI patient regains respiratory effort, the waveform develops a “divot”
“Divot” reflects patient’s inspiratory effort
Important in judging neurological status, or in the presence of therapeutic hypothermia protocols post cardiac arrest
May need additional sedatives / paralytics

30. Optimizing Ventilation in Head Traumas
CO2 has profound affect on cerebral blood flow (CBF) & intracranial pressures (ICP)
Treatment goal to titrate & maintain “therapeutic” ETCO2 which directly affects ICP in patients sensitive to fluctuations
Head trauma, Stroke / Intracranial Hemorrhage, Brain Tumors, CNS Infections
Hyperventilation no longer recommended to lower ICP
May decreased cardiac output, which decreases cerebral blood flow & ICP

31. Head Trauma Ventilation Goals
Current critical care recommendations (Class IIa) are to ventilate head trauma patients to achieve normocarbia
ETCO mmHG causes mild cerebral vasoconstriction decreasing ICP
Hypoventilation increases CO2 levels
Increases cerebral hypoxia which causes cerebral vasodilation
Cerebral hypoxia increases CBF to counter cerebral hypoxia, but increased CBF increases ICP which worsens brain edema & secondary brain injury
Hyperventilation decreases CO2 levels
Causes cerebral vasoconstriction decreasing ICP, but increases cerebral hypoxia

32. Non-Intubated Patients
Objectively assess respiratory disorders & response to treatment
Assess hypoventilation severity:
OD (sedatives, hyponotics)
Respiratory distress (CHF, bronchospasm, PE)
Procedural sedation & analgesia
CVA, ICH, Head Injury
Assess hypoperfusion severity:
Shock (medical, traumatic), arrest states
Sepsis
DKA

33. Non-Intubated Patients
Identify problem
Assess patient’s status & anticipate sudden changes
Monitor treatments for respiratory, medical & traumatic processes
Ventilation: movement of gases in & out of lungs
Diffusion: gas exchange between oxygenated alveoli & pulmonary circulation
Perfusion: blood circulation through arterial & venous systems

34. Oxygenation, Ventilation & Perfusion
Oxygenation: Process of getting O2 into the body
Ventilation:
Process of eliminating CO2 from the body
Perfusion:
Process of getting oxygenated blood into an organ or body

35. Ventilation-Perfusion Mismatch
Ratio of the amount of O2 reaching alveoli to amount of blood reaching alveoli
"V" = ventilation (air reaching alveoli)
"Q" = perfusion (blood reaching alveoli)
High Ratio
Limited O2 / gas exchange due to impaired blood flow (i.e. “dead space”)
Low ETCO2, low to normal O2
Example: Pulmonary embolism
Low Ratio
Bloodflow adequate for gas exchange, but not enough alveolar airflow
High ETCO2, low O2
Examples: asthma, COPD, CHF, pulmonary edema

36. DEAD SPACE VENTILATION VQ MISMATCH / SHUNT PERFUSION
Ventilation without perfusion
As no gas exchange occurs, air coming out is the same as air going in (no CO2 exhaled)
Clinically suspect:
Hypotension
Pulmonary embolism
Emphysema
Bronchopulmonary dysplasia
Cardiac arrest
Perfusion without ventilation
Effect on ETCO2 may be small but oxygenation may decrease greatly
Clinically suspect:
Bronchial intubation
Increased secretions
Mucus plugging
Bronchospasm
Atelectasis

37. Non-Intubated Patient: Ventilation
Movement of gases in & out of the lungs which may be restricted or obstructed from many processes
Smooth muscle contraction
Bronchospasm
Airway narrowing
Uneven emptying of alveoli
Mucous plugs
Patients can have several alterations in their ventilatory status. One that is of frequent concern in EMS is:
Airway obstruction such as in:
Smooth muscle contraction
Bronchospasm
Airway narrowing
Uneven emptying of the alveoli
Mucous plugs
Capnography is useful in monitoring your patient’s airway.

38. Non-Intubated Patient: Diffusion
Gas exchange between air-filled alveoli & pulmonary circulation
Inflammation
Retained secretions
Fibrosis
Decreased compliance of alveoli walls
Chronic airway modeling (COPD)
Reversible airway disease (asthma)

39. Bronchospasm
Airway irregularities lead to uneven emptying of alveolar gas / air flow
Alveoli unevenly filled & emptied on inspiration & exhalation
Asynchronous flow dilutes exhaled CO2 (Slower rise in CO2 concentration during exhalation )
Changes ascending phase (II) with loss of sharp upslope & alveolar plateau (III) producing a “shark fin” appearance

40. Bronchospasm: Asthma Asthma costs in the US $56 billion annually
10.5 million missed school days
14.2 million missed work days
Prevalence increased 75% from
2002: 18.7 million adults (1 in 12)
2002: 7 million children (1 in 11)
2-3 million ED visits, 7 million outpatient visits annually
25% asthmatic pediatrics have >1 ED visit annually
Most common chronic pediatric health problem with increasing hospitalizations & deaths
~9 people die from asthma daily
Sources: Delbridge T., et al Prehospital Asthma Management. Prehospital Emergency Care 7 (1) 42-47
Asthmatic Statistics. American Academy of Allergies, Asthma and Immunology. http.//

41. Asthma Pathophysiology
Hyper-reactive airway response to a reversible obstructive process
Release of inflammatory mediators (histamine, bradykinin prostaglandin) increases airway inflammation & edema
Bronchial wall reaction causes reversible obstruction
Spasm of bronchial smooth muscle
Vasodilatation with swelling of bronchial mucous membranes
Increased mucous production

42. Asthma Waveform
Normal
Expiratory airflow obstruction affects shape of the CO2 time curve due to uneven alveolar gas emptying of alveolar gas
Waveform examples show increasing change in normal expiratory plateau with increasing obstruction / bronchospasm
Bronchospasm

43. COPD
Spectrum of diseases with major risk factors being: smoking, exposure to dusts /fumes, frequent respiratory infections
4th leading cause of death (adults)
Annual deaths doubling in past 25 years
Chronic, progressive, partially reversible obstructive process
Inflammation causes excess mucous production, fibrosis, hyperplasia of mucus glands & smooth muscle
Chronic alveolar damage causes hyperinflation due to air trapping, impairs air exchange
Hyper-reactive airway (bronchospasm)
Often have other cardiac & metabolic abnormalities (CAD, CHF, DM, HTN)

44. Capnography in COPD
Normal
Arterial CO2 (PaCO2) increases as disease progresses as patients retain metabolic waste
Ascending phase and plateau are altered by uneven emptying of gases, similar to acute asthmatics
COPD 4 5

45. Hypoventilation 4 5 Elevated ETCO2 (often >50mmHG)
Elevated ETCO2 (often >50mmHG)
Box-like waveform shape unchanged, just height & time
Longer time to “blow off” CO2
Higher levels of CO2 due to retention
Seen in :
Sedation
Intoxication / Ingestions
Stroke / Head Injury
CNS infections 4 5

46. Hypoperfusion Pulmonary blood flow Systemic perfusion Cardiac outputx y g e n 2 V i A t
Pulmonary blood flow
Pulmonary emboli (V/Q mismatch)
Systemic perfusion
Sepsis
Hypovolemia
DKA
Trauma
Cardiac output MI
CHF
Arrhythmia

47. Pulmonary Embolus
Typical: CP, SOB, tachycardia & unilateral lower extremity swelling (DVT)
May have normal oxygenation
Risk factors:
Contraceptives
Prolonged stasis (i.e. travel)
Cancer
Limited mobility
Hx of DVT / prior PE
Decreased alveolar perfusion causes low ETCO2 (V/Q mismatch)

48. Seizure Patients
Patients may be actively seizing & have “normal” respirations for a period of time
In seizing patients a low ETCO2 indicates inadequate respirations
Useful in patients with pseudoseizures

49. Metabolic Conditions Elevated ETCO2 (>50mmHg) seen in hyperthermia4 5
Elevated ETCO2 (>50mmHg) seen in hyperthermia
Low ETCO2 (<29 mmHg) associated with metabolic acidosis
CO poisoning, hypothermia, DKA
If patient in DKA, ETCO2 level will be often be low
2002 study: 95% diabetic children presenting to ED with ETCO2 <29mmHg were in DKA
Elevated ETCO2 in DKA with respiratory compensation or Kussmaul’s
Waveform rapid / slow, but normal shape (not restrictive/ obstructive)

50. WAVEFORM REVIEW & CASE STUDIES

51. Capnography Waveform 1 waveform = 1 respiratory cycle
Height = amount of CO2
Length = time of respiratory cycle
Information in 4 second views; Printouts in “real-time” views
Baseline usually “0” as no CO2 normally present during inspiration
Normal range is 35-45mm Hg (5% vol)

52. Quick Review: Normal Capnograph
Waveform begins at a “0” baseline, raises steeply, plateaus with a gradual upslope, & quickly returns to the “0” baseline
ETCO2 reading within the normal range of mmHg

53. Quick Review: Bronchospasm
The loss of a slightly upsloping alveolar plateau indicates an incomplete or obstructed exhalation
Waveform often has a “shark fin” pattern indicating that exhalation is slowed, often by bronchoconstriction
Common causes include asthma, COPD, or an airway obstruction

54. Quick Review: Hypoventilation
Increasing ETCO2, though waveform retains a fairly normal shape
Patients not breathing fast enough or deep enough to adequately remove CO2 from the lungs, resulting in increasing ETCO2
Seen in decreased respiratory drive due to narcotic OD, CNS depression, or sedation

55. Quick Review: Apnea Sudden loss of a waveform indicates no CO2 present
In spontaneously breathing patient ~ patient stopped breathing / respiratory arrest or equipment has malfunctioned
If advanced airway in place, this indicates there is a problem with the airway itself (displaced or obstructed)

56. Quick Review: Esophageal Intubation
A normal capnograph is best evidence that the ETT correctly positioned & proper ventilation occurring
When ETT placed in esophagus, either no CO2 sensed or only small transient waveforms are initially present
ETCO2 verification considered “standard” for proper airway placement

57. Quick Review: Air Trapping
Baseline elevation indicates there is incomplete inhalation &/or exhalation (CO2 not completely washed out during inhalation)
Often seen with air trapping in (history of asthma or COPD), or a malfunction in the BVM or ventilator exhalation valve
Increasing expiratory time helps remove excess CO2

58. Quick Review: Hyperventilation
The capnograph initially appears normal
Waveforms become closer together & the level of ETCO2 decreases as respiratory rate increases
When decreasing CO2 levels are noted, slow the BVM ventilation (if intubated)
In the spontaneously breathing patient, increasing respiratory rate and decreasing end tidal CO2 levels can be a sign of PE

59. Quick Waveform Review Normal Hyperventilation Hypoventilation45
Normal 45
Hyperventilation 45
Hypoventilation 45
Bronchospasm

60. Case Study 1 4 5 3 2
88yo M with CC of “Short of breath” over the past week, now acutely worse. Already on home O2, taking multiple nebs
PMH: MI, COPD, CHF, DM
Vitals: HR 60, BP 110/70, RR 36 labored/shallow, O2 72% (2L), ETCO2 17mmHG
Exam: Wheezing, rales, rhonchi through pursed lips. Skin cool/diaphoretic, pitting edema BL
The following waveform is noted (see above). What is your diagnosis (or diagnoses) & treatment?
Hyperventilation, no bronchospasm waveform shape. Improvement with treatment (rising CO2 levels). Likely CHF rather than COPD

61. Case Study 2
Hypoxic 82 yo F, NH patient on 2 L via NC, in profound distress, drowsy, lethargic, but alert to name
PMH indicates she is a “Full Code”, with metastatic bone cancer on multiple medications for pain, CHF, HTN, dementia & AFib
Vitals: SpO2: 82%, RR: 40bpm, HR: 130bpm / irregular, BP: 107/48
EKG : presented
Exam: rousable to name, no focal motor / sensory findings, no evidence of recent trauma. Pupils:

62. Hypoventilation due to narcotics
Case Study 2 Continued
Waveform is as above:
What clinical condition(s) is exam, EKG & waveform consistent with?
What would your immediate treatment(s) be to help with the respiratory distress
Hypoventilation due to narcotics

63. Hypovolemia Due To Trauma
Case Study 3
Hypovolemia Due To Trauma
23 yo M involved in a high speed MVC in which he is currently entrapped. Helicopter called while patient extricated & stabilized.
Exam shows obvious chest & lower extremity trauma, though pulses are intact distally (weak / equal / present BL). Patient is A&Ox3 but lethargic
Vitals: HR 120 / reg; SBP 80, O2 sat 98%. While establishing IV, you place a NC on patient with side-stream capnography which shows the following:
What is your assessment? How does this help you clinically?
Let’s look at a case scenario of a patient with low perfusion.
• 57 year old male
• Auto crash with injury to chest
• History of atrial fib, anticoagulant
• Unresponsive
• Pulse 100 irregular, BP 88/p
• Intubated on scene

64. Case Study 4 Dislodged / Kinked ETT
You successfully intubated a patient in respiratory distress secondary to CHF with confirmed ETCO2 & a good waveform after Duonebs, lasix & nitroglycerin
Even though patient’s oxygenation remains in the high 80s / low 90s, you note a sudden loss of waveform decreasing to near 0
What happened?
Dislodged / Kinked ETT

65. Case Study 5
You are transferring a patient from your stretcher to the ED’s bed
Though the waveform had been normal, with levels in the range, after transfer, you note the following waveform
What happened?
Absent alveolar plateau indicates incomplete alveolar emptying or loss of airway integrity ~ ETT dislodged, but likely in the hypopharynx or blocked by secretions

66. Case Study 6 Hypoventilation
You have placed ETCO2 on a patient with pinpoint pupils, & a respiratory rate of 8 who is maintaining his airway, though lethargic
He has responded minimally to naloxone, & smells heavily of ETOH
What does the waveform indicate?
Hypoventilation

67. Case Study 7 Hyperventilation
You have been called to the house of a 16 year old girl who has just broken up with her boyfriend
She is hysterical & her mother states that “she is having a bad asthma attack”
He lungs are clear, O2 saturation is 99%, but she does appear to have some respiratory distress
What diagnosis is suggested by upon the waveform?
Hyperventilation

68. Case Study 8
You are resuscitating a patient in VF arrest with just you (“Joe Paramedic”), a driver, & one EMT
The EMT has been doing compressions throughout the transport (10 minutes) when you note the change in waveform
What are two likely scenarios to explain the waveform?
Gradual decreasing ETCO2 with a normal waveform shape (just decreased height) indicated decreased CO2 production (death), hyperventilation (rapid BVM) or decreasing cardiac output resulting in decreased systemic & pulmonary perfusion (ineffective compressions)

69. Case Study 9
18 yo F with 2 days increasing SOB, wheezing, not controlled by her daily asthma medications or her rescue inhaler. Also notes possible peanut exposure with a known peanut allergy
Called to the house to find patient tripodding,stridorous though with minimal wheezing heart. O2 sat 88%, HR 120s, SBP 90 & very anxious.
The following waveform is seen:
What is your immediate assessment & management plan?

70. Continue current care. Waveform & exam indicate the patient improving
Case Study 9
NRB O2 100% applied, IV started, solumedrol given, sub Q epineprine dosed, Duoneb initiated, medical control notified
Within 5 minutes, the O2 saturation is 92%, HR in the 130s with patient remaining anxious but alert. SBP now 110 & the following waveform is seen:
What is your plan?
1st Waveform
Continue current care. Waveform & exam indicate the patient improving
2nd Waveform

71. Meet Howard Snitzer
54 yo male with a VF arrest in January 2011 in rural Minnesota which serves as a case study as to why to continue a “futile resuscitation”
2 dozens rescuers took turns providing CPR for 96 minutes during his prolonged transport with periods of VF, PEA, asystole
6 shocks by 1st responders, 6 more shocks by Mayo Air Flight on way to cath lab
Had thrombectomy & stent to LAD, spent 10 days in Mayo Clinic
Why did the rescuers continue when there were no signs of life?
“The capnography told us not to give up” …ETCO2 averaged 35 during entire resuscitation

72. References EMSWorld.com. “Waveform Capnography” 2009.
Bonner County EMS “Waveform Capnography”
Medtronic “Capnography in Emergency Care”
English J, Pointer J, Jacobs M. “Capnography: The Standard of Care”. 2005
Guidelines for Cardiovascular Resuscitation and Emergency Cardiovascular Care, Circulation 102 (suppl I) 8. August 22,2010
Wayne MA, Levine RL, Miller CC. “Use of End-tidal Carbon Dioxide to Predict Outcome in Prehospital Cardiac Arrest” . Annals of Emergency Medicine. 1995; 25(6):
Levine RL., Wayne MA., Miller CC. “End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest.” New England Journal of Medicine. 1997;337(5):
Cummins RO. Principles & Practice. American Heart Association
Weil MH Cardiac output and ETCO2. Critical Care Medicine 13 (11):
Ochoa F. et al The Effect of Rescuer Fatigue on Quality of Chest Compressions. Resuscitation April; 37:
White RD. Out-of-Hospital Monitoring of ETCO2 Pressure During CPR. AEM (1):
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73. Summary prehospitalmd@gmail.com
Visual objective measure of ventilation
Breath-to-breath readings for intubated & non-intubated patients
Clinical information to guide patient care
Objective documentation