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Continuous Capnography ~
The “Wave” of the Future
Amy Gutman MD ~ EMS Medical Director
[email protected]
Objectives
 What is the capnogram?
 Review capnogram appearance
in relation to physiology with
clinical implications
 Incorporate capnography into
protocols
Appreciation to Medtronics for 2010 permission to use portions of their training module in preparing this presentation
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
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
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)
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
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)
OXYGENTATION
 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
VENTILATION
 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
Capnogram from www.emscapnographyblogspot.com
INCREASED 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
DECREASED ETCO2
 METABOLISM
 Hypothermia
 Metabolic Acidosis
 Decreased muscular activity
 RESPIRATORY
 Hyperventilation
 Bronchospasm
 Mucus Plugging / Obstruction
 CIRCULATORY




Decreased cardiac output
Shock states
Cardiac Arrest
Pulmonary Emboli
Capnography Waveform
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 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)
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
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
Alveoli
C
B
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
C
D
Capnogram Phase IV:
Descending Phase
• Inhalation / Inspiration begins & O2
rapidly fills the airways
• CO2 level quickly drops to “0” baseline
Alveoli
D
E
ETCO2 Monitoring
 Airway
 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
Clinical Capnography
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.
Intubated Patients (Non-Arrest)
 Verify & continuously confirm ETT
placement
 Immediately detect ETT position
changes
 Optimize ventilation management
ETT Placement Confirmation*
Annals
2005; 45:497-503
 Standard of
care of
forEM
confirmation
& monitoring
of the intubated patient is waveform
capnography,
oximetry,
& physical
No pulse
unrecognized
misplaced
confirmation
(i.e. auscultation,
tube found
fog) in
endotracheal
intubations were
patients for whom paramedics used
 Presence continuous
of exhaled CO
tracheal
2 indicates
ETCO
2 monitoring.
placement within seconds of proper placement
 Esophageal ETT placement may briefly detect CO2
Failure“washed
to use continuous
but residuals
out” within 6ETCO
positive2
pressure
ventilations
monitoring
associated with a 23%
 Gastric CO2 from: carbonated beverages, Tums,
unrecognized
rate
gastric
distention misplaced
from mouthintubation
to mouth ventilation
*Guidelines 2000 for Cardiovascular Resuscitation & Emergency Cardiovascular Care, Circulation. August,2000
ETT Displacement
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 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
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)
 Silvestri S. “Improvement in Misplaced
ETT Recognition within a Regional EMS
System” (AEM. 2003)
 108 patients intubated in the field
 52 trauma, 56 medical patients
 108 patients intubated in the field
 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
 9% had improperly placed ETT
 No unrecognized misplaced ETT in
pts with continuous ETCO2 monitoring
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
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
Rescuer Fatigue &
Compressions
 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
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Detecting ROSC
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0
 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.
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
 90 medical OOHCA PEA patients
 ETCO2 90% sensitive in predicting
ROSC
 100% mortality if unable to achieve
ETCO2 >10mmHg after 20 minutes
 Maximal ETCO2 <10mmHg during
1st 20 minutes after intubation
never associated with ROSC (0%)
 16 survivors
90%
80%
70%
60%
50%
40%
30%
20%
10%
0%
survival
 In 13 survivors a rapid rise of ETCO2
was earliest ROSC indicator
 1-3 mins before palpable pulse
 3-7 mins prior blood pressure
10-12
min
20 min
30 min
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
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
Head Trauma
Ventilation Goals
 Current critical care recommendations (Class IIa) are to ventilate head
trauma patients to achieve normocarbia
 ETCO2 25-30mmHG 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
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
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
Oxygenation, Ventilation & Perfusion
Oxygenation:
Process of getting
O2 into the body
Perfusion:
Process of getting
oxygenated blood into an
organ or body
Ventilation:
Process of eliminating
CO2 from the body
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
DEAD SPACE VENTILATION
VQ MISMATCH / SHUNT PERFUSION
 Ventilation without perfusion
 Perfusion without ventilation
 As no gas exchange occurs, air
coming out is the same as air going
in (no CO2 exhaled)
 Effect on ETCO2 may be small but
oxygenation may decrease greatly
 Clinically suspect:
 Hypotension
 Pulmonary embolism
 Emphysema
 Bronchopulmonary dysplasia
 Cardiac arrest
 Clinically suspect:
 Bronchial intubation
 Increased secretions
 Mucus plugging
 Bronchospasm
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
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)
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
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 1980-1994
 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
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
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
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)
Capnography in COPD
 Arterial CO2 (PaCO2)
increases as disease
progresses as patients retain
metabolic waste
Normal
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COPD
 Ascending phase and plateau
are altered by uneven
emptying of gases, similar to
acute asthmatics
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Hypoventilation
 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
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45
0
Hypoperfusion
 Pulmonary blood flow
Artery
Oxygen
 Pulmonary emboli (V/Q mismatch)
 Systemic perfusion




Sepsis
Hypovolemia
DKA
Trauma
 Cardiac output
 MI
 CHF
 Arrhythmia
O2
Vein
Pulmonary Embolus
45
35
25
0
 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)
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
Metabolic
Conditions
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 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)
WAVEFORM REVIEW &
CASE STUDIES
Capnography Waveform
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 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)
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 35-45 mmHg
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
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
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)
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
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
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
Quick Waveform Review
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0
45
0
45
0
45
0
Normal
Hyperventilation
Hypoventilation
Bronchospasm
Case Study 1
45
35
25
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 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?
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:
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
Case Study 3
45
35
25
0
 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?
Case Study 4
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?
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
35-40 range, after transfer, you note the following
waveform
 What happened?
Case Study 6
 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?
Case Study 7
 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?
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?
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?
Case Study 9
 NRB O2 100% applied, IV started,
solumedrol given, sub Q
epineprine dosed, Duoneb
initiated, medical control notified
1st Waveform
 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?
2nd Waveform
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
References
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EMSWorld.com. “Waveform Capnography” 2009.
Bonner County EMS “Waveform Capnography”. 2010.
Medtronic “Capnography in Emergency Care”. 2008.
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
www.emscapnographyblogspot.com
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):762-767.
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):301-306.
Cummins RO. Principles & Practice. American Heart Association. 2003.
Weil MH. 1985. Cardiac output and ETCO2. Critical Care Medicine 13 (11): 907-909
Ochoa F. et al. 1998. The Effect of Rescuer Fatigue on Quality of Chest Compressions. Resuscitation April; 37: 149-52
White RD. Out-of-Hospital Monitoring of ETCO2 Pressure During CPR. AEM. 199423 (1): 756-761
Levine R. L. ETCO2 & outcome of OOHCA. NEJM.1997. 337 (5): 301-306.
Huizenga JE. Guidelines for the Management of Severe Head Injury: Are Emergency Physicians Following Them? AEM. 2000. 9 (8): 806-812
Asthmatic Statistics. American Academy of Allergies, Asthma and Immunology. www.aaaai.org
Hall J.B., Acute Asthma, Assessment and Management, McGraw-Hill, New York.
Falk J. 1988. ETCO2 concentration during CPR. NEJM. 318 (10): 607-611
Flanagan, J.F., et al. 1995. Noninvasive monitoring of ETCO2tension via nasal cannulas in spontaneously breathing children with profound hypocarbia.
Critical Care Medicine. June; 23 (6): 1140-1142
Delbridge T, et al. 2003 Prehospital Asthma Management. PEC. 7(1) 42-47
Capnography: The Standard of Care. JEnglish, J Pointer, M Jacobs, EMT-P. A;lameda Public Health Department.
Hanley C. Perianesthesia Nurses Association of British Columbia. “Capnography in the PACU: Theory and Clinical Applications of end tidal C02
Monitoring”. 2010.
McEvoy M. Capnography Could Make You a Rock Star! CTICU and Resuscitation Committee Chair Albany Medical Center. 2011.
Summary
[email protected]
 Visual objective measure of
ventilation
 Breath-to-breath readings for
intubated & non-intubated patients
 Clinical information to guide patient
care
 Objective documentation