End-Tidal CO₂ Monitoring in Critical Care

Thompson Health  |  F.F. Thompson Hospital  |  Nursing Education — Critical Care

Welcome to This Module

The number on the capnography screen is only as useful as your ability to interpret it. This module builds that foundation — the physiology that explains why EtCO₂ changes, what a good waveform looks like versus a concerning one, and how to use that information confidently at the bedside during resuscitation and in continuous monitoring.

Complete all six content modules, then pass the knowledge assessment with a score of 80% or higher to receive credit.

📚 Learning Objectives After completing this module, you will be able to:
  1. Explain the physiology of CO₂ production, transport, and elimination as it relates to EtCO₂ values.
  2. Interpret capnography waveforms and numerical EtCO₂ values at the bedside and during resuscitation.
  3. Use continuous EtCO₂ monitoring to detect opioid-induced respiratory depression, hypoventilation, and deterioration earlier than pulse oximetry.
  4. Correctly set up and troubleshoot EtCO₂ monitoring on the GE CARESCAPE B650 with E-miniC module at the bedside.
  5. Use EtCO₂ to assess CPR quality, recognize ROSC, and support resuscitation decisions.
  6. Apply post-resuscitation EtCO₂ targets to guide ventilation management and protect neurologic outcomes.
  7. Correctly set up and operate EtCO₂ monitoring on the Stryker LIFEPAK 15 during a code.

Module Map

StepModuleTopic
11EtCO₂ Basics & Physiology
22Continuous Bedside Monitoring
33GE CARESCAPE B650: Setup & Operation
46LIFEPAK 15: Setup & Operation
54EtCO₂ During CPR & Resuscitation
65Post-Resuscitation Care
——Knowledge Assessment (12 questions)
💡 Navigation Tip Use the tabs above to move between modules, or use the Next/Previous buttons at the bottom of each page. Complete all modules before beginning the assessment.
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Module 1: EtCO₂ Basics & Physiology

What Is EtCO₂?

End-tidal carbon dioxide (EtCO₂) is the concentration of carbon dioxide (CO₂) measured at the very end of a patient's exhaled breath — the point at which the gas most closely represents alveolar (lung) CO₂. It is measured in millimeters of mercury (mmHg) or as a percentage (%).

Capnometry refers to displaying EtCO₂ as a number. Capnography refers to displaying both the numeric value and a continuous waveform tracing. Capnography provides significantly more clinical information and is the preferred method in critical care.

35–45
Normal EtCO₂ (mmHg)
4.7–6.0
Normal EtCO₂ (kPa)
5–6%
Normal EtCO₂ (Vol%)
1–5
Normal PaCO₂–EtCO₂ gradient (mmHg)
🔬 Physiological Connection Under normal conditions, EtCO₂ closely approximates arterial CO₂ (PaCO₂). EtCO₂ is typically 1–5 mmHg lower than PaCO₂ due to dilution with dead-space gas. When ventilation-perfusion (V/Q) matching is abnormal — as in critically ill patients — this gradient may widen significantly, and arterial blood gas correlation becomes essential.

The Physiology Behind the Number

CO₂ is a byproduct of cellular aerobic metabolism. For EtCO₂ to be detected at the airway, three physiological processes must function together:

  • Metabolic production: Cells produce CO₂ as they burn fuel for energy. Changes in metabolic rate (fever, shivering, exercise, sepsis) alter CO₂ production.
  • Circulatory transport: CO₂ is carried in the bloodstream to the pulmonary capillaries. During cardiac arrest or states of very low cardiac output, CO₂ cannot reach the lungs even if it is being produced — the EtCO₂ falls. This is why EtCO₂ is a valuable surrogate for cardiac output during CPR.
  • Alveolar ventilation: CO₂ must be effectively eliminated through the lungs. Hypoventilation causes CO₂ to rise; hyperventilation causes it to fall.
⚠️ EtCO₂ vs. Pulse Oximetry SpO₂ measures oxygenation, not ventilation. In a patient receiving supplemental oxygen, SpO₂ may remain normal for many minutes even as the patient hypoventilates and CO₂ rises dangerously. EtCO₂ detects hypoventilation and respiratory depression earlier than pulse oximetry — before SpO₂ drops.

How Is EtCO₂ Measured?

There are two primary sampling methods:

MethodHow It WorksBest Used For
Mainstream (Inline)Sensor sits directly at the patient-ventilator interface; measures CO₂ in real timeIntubated, ventilated patients; fastest response
Sidestream (Diverting)Small-bore tubing (FilterLine) draws a gas sample (50 mL/min) to the monitor for analysisIntubated and non-intubated patients; includes oral-nasal cannulas

The LIFEPAK 15 uses Microstream® sidestream technology with a FilterLine sampling set. The low flow rate (50 mL/min) and micro-sample size (15 µL) reduce obstruction by fluids and maintain waveform quality even at high respiratory rates.

The Normal Capnography Waveform

A normal capnogram has a characteristic rectangular shape. Learning to interpret the waveform — not just the number — is essential to accurate assessment.

45 20 0 I — Baseline II — Upstroke III — Plateau D = EtCO₂ IV — Downstroke A B C E mmHg
Normal capnography waveform — two respiratory cycles shown. Labels mark Cycle 1 phases.
Interactive: Explore how ventilation affects EtCO₂ EtCO₂40 mmHg
Live waveform unavailable in this browser. Use the phase diagram above for reference.
Normal
LowNormalHigh
Normal rectangular capnogram with a flat Phase III plateau and EtCO₂ around 40 mmHg — what you want to see.
PhaseSegmentWhat It RepresentsNormal Appearance
I — Respiratory BaselineA → BExhalation of CO₂-free dead-space gasFlat line at zero
II — Expiratory UpstrokeB → CMix of dead-space and alveolar gasSharp, steep rise
III — Alveolar PlateauC → DMostly alveolar gasNearly horizontal plateau
Point D — EtCO₂ ValueDMaximum CO₂ at end of exhalation — the recorded valuePeak of waveform
IV — Inspiratory DownstrokeD → EInspiration; CO₂-free gas enters airwayNear-vertical drop back to zero
🔎 Quick Check — Before you scroll on
A patient's EtCO₂ waveform shows a normal Phase I baseline but the plateau (Phase III) slopes upward in a "shark fin" shape. The number reads 38. What's the most likely clinical picture?
The number looks normal, but the waveform tells the real story. An upward-sloping Phase III plateau — the "shark fin" — indicates uneven alveolar emptying from airflow obstruction. Think bronchospasm, asthma, COPD, or partial ETT obstruction. Assess for wheezing and treat the cause — don't be reassured by the number.
🔴 Critical Practice Point Never accept a numerical EtCO₂ value without first examining the waveform. A number without a quality waveform is misleading. An elevated baseline, slanted plateau, or flat-line at zero each tell a different clinical story that the number alone cannot reveal.

Abnormal Waveform Patterns

A flat line at zero means no CO₂ is reaching the sensor. In an intubated patient, immediately assess for: ETT dislodgment or esophageal intubation, disconnection of the FilterLine, cardiac arrest/loss of perfusion, or equipment failure (blocked or kinked tubing). This is always an emergency assessment.
The baseline (Phase I) is elevated above zero. This indicates the patient is rebreathing exhaled CO₂ — commonly caused by increased dead space, an exhausted CO₂ absorber (in rebreather circuits), or hypoventilation. EtCO₂ values also gradually rise. Sensor contamination can cause a sudden, severe baseline elevation.
The alveolar plateau (Phase III) slopes upward instead of remaining flat. This pattern indicates uneven emptying of the alveoli due to airflow obstruction. Common causes include bronchospasm, asthma, COPD, and partial ETT obstruction or kinking. Also known as the "shark fin" waveform. Assess for wheezing and treat bronchospasm.
A progressive decline in EtCO₂ may indicate: decreasing cardiac output, increasing dead space (PE, hypovolemia), hyperventilation, or hypothermia. During CPR, declining EtCO₂ despite continued compressions suggests poor coronary and pulmonary perfusion.
🎯 Pattern Match — Which waveform is this?
Click the waveform that matches: Bronchospasm / severe asthma
📋 Clinical Scenario — Think First
Your post-op patient is 2 hours out of a laparoscopic procedure, on a hydromorphone PCA. SpO₂ is 96% on 2L NC. They're sleepy but arousable. The bedside monitor's EtCO₂ reads 58 mmHg with an upward-drifting trend.
What would you do?
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Module 2: Continuous Bedside EtCO₂ Monitoring

🏥 The Bedside Setup at Thompson Health In the Thompson ICU, continuous bedside EtCO₂ is monitored on the GE CARESCAPE B650 with the E-miniC airway gas module. That is the device you'll use for every patient described in this module. The hands-on setup, water trap, and alarm steps for the B650 are covered in detail in Module 3 (next); this module focuses on when and why to use continuous capnography at the bedside, and how to act on what you see.

When to Use Continuous EtCO₂ Monitoring

A patient can be quietly hypoventilating for 10 minutes before their SpO₂ drops — if they're on supplemental oxygen. That's the gap EtCO₂ monitoring closes. Here's when to use it and what to do with what you see.

Continuous capnography provides ongoing, real-time assessment of ventilation. In the ICU, primary indications include:

  • All intubated and mechanically ventilated patients — particularly during weaning
  • Patients at high risk for opioid-induced respiratory depression (OIRD) — including those on IV opioid infusions, PCA, high-dose oral opioids, or who have obesity, OSA, or advanced age
  • Patients with neurological impairment or altered level of consciousness
  • Procedural sedation and post-procedure monitoring
  • Patients following resuscitation (post-ROSC)
🏥 Evidence: OIRD & Capnography Carlisle (2015) demonstrated that continuous capnography detects opioid-induced respiratory depression significantly earlier than either visual assessment or pulse oximetry. In patients on supplemental oxygen, SpO₂ provides a false sense of security — EtCO₂ is clearly superior for detecting hypoventilation. After implementing a capnography protocol, the number of patients monitored increased 2.56-fold, and opioid-related sentinel events dropped to zero.

Setup: Intubated Patients

For intubated patients, use a sidestream FilterLine set connected to the endotracheal tube (ETT) adapter. Ensure:

  • The sampling port is positioned as close to the patient's airway as possible
  • The adapter is kept upright per manufacturer recommendations to prevent fluid pooling
  • The FilterLine tubing is not kinked or occluded
  • FilterLine sets are for single patient use only — do not reuse

Setup: Non-Intubated Patients

For non-intubated patients, use an oral-nasal sampling cannula (combined CO₂ and O₂ delivery cannula). Position the sampling prongs in the nares and the oral sample port near the mouth. Instruct the patient that it is a safety monitoring device — most patients will cooperate once the purpose is explained.

💡 Patient Adherence Up to 65% of patients complain about the EtCO₂ tubing (Carlisle, 2015). However, 90% of patients will accept monitoring when nurses explain its safety purpose clearly. Take a moment to say: "This small tube helps me make sure your breathing stays safe — it's important for your safety while you're receiving pain medication."

Interpreting EtCO₂ Values at the Bedside

<35
Hypocapnia (mmHg)
Hyperventilation
35–45
Normal Range (mmHg)
46–55
Mild Hypercapnia
Hypoventilation
>55
Significant Hypercapnia
Respiratory failure

Common EtCO₂ Waveform Abnormalities

PatternAppearanceLikely CauseNursing Action
Elevated baselineBaseline >2–3 mmHg above zeroRebreathing CO₂; dead space; equipment contaminationCheck circuit/tubing; notify provider
Shark fin (slanted plateau)Phase III slopes upward (no flat plateau)Bronchospasm, asthma, COPD, partial obstructionAssess for wheezing; consider bronchodilator; notify provider
Gradual rising EtCO₂Values steadily increasingHypoventilation, oversedation, opioid effect, respiratory fatigueStimulate patient; reduce sedation if appropriate; notify provider urgently
Gradual falling EtCO₂Values steadily decreasingHyperventilation, decreasing cardiac output, increasing dead space (PE)Correlate with clinical status; check ABG; notify provider
Sudden drop to zeroFlat line, no waveformETT dislodgment, disconnection, cardiac arrest, equipment failureImmediately assess patient; check ETT placement; check connection
Cleft in plateauNotch or dip in Phase IIISpontaneous respiratory effort against ventilatorAssess patient-ventilator synchrony; notify respiratory therapy

Alarm Management

Set alarm parameters when you start monitoring and reassess them at each shift assessment. This module uses standard patient-specific alarm management: start with clinically reasonable limits, then adjust for the patient's baseline, the reason for monitoring, and any provider orders.

Alarm TypeStandard Starting PointClinical Significance
EtCO₂ HighCommon adult starting range: 50–55 mmHg; individualize for chronic hypercapnia or a specific ventilation goalHypoventilation, respiratory depression
EtCO₂ LowCommon adult starting range: 25–30 mmHg; individualize during CPR, post-ROSC care, or known low baseline valuesHyperventilation, decreasing cardiac output
Apnea / No Breath delay (GE B650)Use the active monitor profile and treat any apnea/no-breath alarm as urgent; do not extend delays casuallyNo breath detected — respiratory emergency
RR High / RR Low (GE B650)Set patient-appropriate high and low limits based on clinical condition, ventilator mode, and monitoring goalRespiratory rate outside target range
No Breath / Apnea (LP15)Automatic — fixed at 30 seconds, not adjustableNo breath for 30 seconds — urgent
FiCO₂ (LP15)Automatic — not adjustableInspired CO₂ above threshold — rebreathing

If alarm limits are changed from the usual patient-specific range, document the reason and reassess whether the new limits are still appropriate as the patient's condition changes. For example: "EtCO₂ high limit increased to 60 mmHg per provider order — chronic hypercapnia, baseline PaCO₂ 58."

🚨 Always Respond to Alarms Never silence an EtCO₂ alarm without first assessing the patient. A NO BREATH alarm in a sedated or opioid-medicated patient must be treated as a respiratory emergency until proven otherwise.
📞 OIRD Escalation: Standard Bedside Response When EtCO₂ indicates opioid-induced respiratory depression (rising trend, EtCO₂ >50 mmHg with decreasing LOC, or NO BREATH alarm on a patient receiving opioids/PCA):
  • Stimulate the patient, open the airway, and apply supplemental O₂ if not already in place.
  • Pause or stop opioid delivery when patient safety requires it while escalating through the current order set, provider, rapid response, or chain-of-command process.
  • Call for immediate help using the unit's rapid response/provider escalation workflow.
  • Have naloxone available if opioid reversal is being considered; administer per active order, standing order, or rapid response direction.
  • Document the EtCO₂ trend, time of escalation, interventions, and response.

Documentation

Document EtCO₂ with routine respiratory/vital-sign assessment, whenever monitoring is initiated or discontinued, and any time the EtCO₂ value, waveform, or alarm response changes care.

  • EtCO₂ value (mmHg) and trend direction
  • Waveform quality (normal, abnormal — describe pattern)
  • Respiratory rate as displayed by the monitor
  • Sampling line type (intubated FilterLine vs. oral-nasal cannula) and site assessment
  • Any alarms triggered and nursing response
  • Patient tolerance of monitoring equipment
🔬 Clinical Pearl (St. John, 2003) Trending the PaCO₂–EtCO₂ gradient over time is more valuable than any single isolated reading. A narrowing gradient suggests improving V/Q matching and pulmonary function. A widening gradient may indicate worsening dead-space, pulmonary embolism, or hemodynamic deterioration — even when the EtCO₂ number looks acceptable.

Device Choice: GE B650 vs. LIFEPAK 15

Thompson has two EtCO₂-capable devices, and they are designed for different phases of care. Knowing which to reach for — and when to switch — is part of safe monitoring.

GE CARESCAPE B650 (bedside)Stryker LIFEPAK 15 (code cart)
Intended useContinuous bedside monitoring over hours to daysTransport, resuscitation, and defibrillation
Sampling flow150 mL/min (E-miniC) — higher flow, faster response to rate changes50 mL/min (Microstream) — lower flow, more tolerant of secretions
StrengthsIntegrated with all the patient's other vitals, alarms, and EHR documentation; can run indefinitelyBuilt into the defibrillator; mobile; designed to keep working through chest compressions and transport
WeaknessesStays at the bedside — can't come with you to CT or a code elsewhere; water trap fills fasterNot meant for long-term continuous monitoring; less integration with other parameters
💡 Switching to the LIFEPAK 15 When a Code is Called If your patient is already on continuous EtCO₂ via the GE B650 and goes into arrest, the code team will bring the LIFEPAK 15 to the bedside. Even though the B650 is still monitoring, it is generally better to transition capnography to the LIFEPAK 15 during the code. Reasons:
  • Integration with compressions and defibrillation. The LP15 is the device the code team is already using for rhythm, shocks, and drug dose timing — having EtCO₂ on the same screen keeps the CPR feedback loop tight.
  • Movement. If the patient needs to move to CT, another care area, or transfer preparation, the LP15 goes with them. The B650 doesn't.
  • Sampling robustness during arrest. The LP15's lower sampling flow and Microstream filter line tolerate secretions, blood, and fluid in the circuit — all of which are common during arrest.
  • Continuity of numeric value. Both devices report EtCO₂ in mmHg. Note the last GE value before you switch and compare to the first LP15 value so the team has a continuous picture of perfusion across the transition.
Practically: unplug the patient end of the GE sampling line (leave the B650 running so the rest of the vitals are still captured), attach a fresh LP15 FilterLine to the ETT or oral-nasal cannula, and announce out loud, "EtCO₂ is now on the LIFEPAK — last value on GE was [X]."

External transfer note: Thompson does not have an in-house cath lab. If the patient needs PCI-capable care, anticipate transfer to Strong. Many EMS services that transport Thompson patients may have EtCO₂-capable monitors, often LIFEPAK or ZOLL, but capability and setup vary by crew. Before disconnecting Thompson monitoring, confirm whether EMS can continue capnography and hand off the last reliable EtCO₂ value and waveform quality.
🔀 Device Chooser — Pick the right monitor
Scenario 1 of 4
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Module 3: EtCO₂ on the GE CARESCAPE B650 Device-Specific Thompson Health ICU

This is the monitor you'll use at the bedside in the Thompson ICU. The CARESCAPE B650 works with a small plug-in module called the E-miniC — that's the white rectangular device that snaps into the side of the monitor. Together, they give you continuous sidestream EtCO₂ monitoring right at the bedside.

💡 What Makes This Different from the LIFEPAK 15 The LIFEPAK 15 is your code cart monitor — great for resuscitation. The CARESCAPE B650 is your continuous bedside monitor for ongoing care. Same EtCO₂ principles apply, but the equipment and setup are a little different. The biggest practical difference: the B650's E-miniC pulls gas at a much higher flow rate, which means the water trap fills up faster and needs more attention.

Your Equipment at a Glance

Before you start, here's what you're working with:

  • GE CARESCAPE B650 monitor — the main bedside monitor
  • GE E-miniC module — already installed in the module slot on the B650. It's a single-width white module about the size of a deck of cards. You can see the gas inlet port and the "Gas Exhaust" label on the front face.
  • Mini D-Fend water trap — a small disposable trap that snaps onto the E-miniC. It catches moisture from the patient's breath before it reaches the sensor. Single-patient use — grab a fresh one from your supplies.
  • Sidestream sampling line — for intubated patients, this connects to the ETT circuit. For non-intubated patients, there's an oral-nasal CO₂ cannula.
150
Gas sampling flow (mL/min) — 3× faster than LIFEPAK 15
4–80
Respiratory rate range detected (breaths/min)
0–150
CO₂ measurement range (mmHg)

Getting It Set Up

The setup takes just a couple of minutes once you're familiar with it. Here's how it goes:

These steps are here as a reference. Focus on understanding when and why to use the device — the step-by-step guide is available any time you need it.
  1. Check that the E-miniC is seated in the B650
    The monitor should already show a CO₂ parameter on screen when the module is properly installed. If you see "CO₂ NO SENSOR," the module may need to be reseated — push it firmly into the slot. If it still doesn't register, remove the monitor from service and contact Biomedical Engineering.
  2. Snap a fresh Mini D-Fend water trap onto the E-miniC
    The water trap connects to the gas inlet on the front of the E-miniC. Push it in firmly until it seats — a loose trap will alarm almost immediately. Water traps are single-patient use, so always start with a new one.
  3. Attach the sidestream sampling line to the water trap
    Connect the sampling line tubing snugly to the outlet end of the water trap. Make sure the connection is tight — a small leak here will give you falsely low EtCO₂ readings even though the monitor shows a waveform.
  4. Wait for the module to initialize
    Once the sampling line is connected, the E-miniC will run a brief self-check. Give it a moment before connecting the patient end — you'll see the CO₂ display become active when it's ready.
  5. Connect to your patient
    Intubated: Connect the sampling line adapter to the ETT Y-piece or swivel adapter. Try to keep the water trap upright — it drains better and lasts longer that way.

    Non-intubated: Place the oral-nasal cannula with the nasal prongs in the nares and the small oral sampling port near the mouth. Route the tubing comfortably over the ear.
  6. Confirm you have a waveform and a number
    You should see a CO₂ waveform trace and an EtCO₂ value (in mmHg) on the B650 screen. The monitor also displays a respiratory rate derived from the CO₂ signal. No waveform? Trace your connections from module to patient — something is likely loose or disconnected.
  7. Set your alarm limits
    Go to the Alarm Setup menu and set EtCO₂ high and low, RR high and low, and apnea/no-breath limits using the active monitor profile and the patient's condition. Common adult EtCO₂ starting points are high around 50–55 mmHg and low around 25–30 mmHg; adjust for baseline, ventilation goals, CPR or post-ROSC context, and provider orders. Document meaningful changes and the clinical reason.
  8. Turn on O₂ compensation if your patient is on more than 40% oxygen
    This step is easy to skip, but it matters. When a patient is on high levels of supplemental oxygen (FiO₂ above 40%), the CO₂ reading can look slightly lower than it actually is — up to about 0.3 vol% off. Go to CO₂ Setup → O₂ Compensation and enter the patient's FiO₂. With compensation on, the error drops to less than 0.15 vol%. Most of your ICU patients will need this step.

About the Water Trap

The water trap is worth a dedicated conversation because it's the most common source of E-miniC alarms in everyday ICU use. The E-miniC draws gas at 150 mL/min — three times faster than the LIFEPAK 15. That higher flow rate means moisture from your patient's breathing fills the trap more quickly, especially in humidified ventilator circuits.

A few habits that help:

  • Check the water trap when you do your shift assessment — if you can see it's getting full, change it rather than waiting for the alarm
  • Keep the trap upright as much as possible — it drains better and blocks less often
  • Replace the water trap between patients, at least daily during ongoing use, and sooner if it is wet, full, contaminated, or causing low-flow/disconnected alarms
  • Replace the sampling line between patients and whenever it is wet, kinked, blocked, soiled, or no longer giving a reliable waveform; use the stocked line compatible with the Mini D-Fend setup
  • If the monitor alarms "WATER TRAP DISCONNECTED" and the trap looks connected — press it in more firmly, it may just be slightly unseated

Alarms You'll See

AlarmWhat It MeansWhat To Do
EtCO₂ HighCO₂ above your set limit — patient may be hypoventilatingAssess the patient; check airway and breathing effort
EtCO₂ LowCO₂ below your set limit — hyperventilation or dropping perfusionAssess the patient; check clinical status; consider ABG
FiCO₂ HighThe patient is rebreathing CO₂ — it's showing up in inspired gasCheck the ventilator circuit; notify provider
RR High / RR LowRespiratory rate outside your set rangeAssess the patient; correlate with their clinical picture
ApneaNo breath detected within the alarm interval — treat as urgentAssess patient immediately — check airway and breathing
Water Trap DisconnectedTrap is loose, full, or not attachedCheck and reseat; replace if full
CO₂ Low Flow / Sample Line BlockedSomething is blocking the gas path — kinked tubing, saturated trapCheck tubing; replace water trap or sampling line

When Things Aren't Working

What You're SeeingMost Likely CauseTry This
"CO₂ NO SENSOR" E-miniC module isn't registering Firmly reseat the module; if it persists, remove the monitor from service and contact Biomedical Engineering
"WATER TRAP DISCONNECTED" Trap is loose or not attached Press the water trap in firmly; replace if it looks full
"CO₂ LOW FLOW" or "CHECK SAMPLING LINE" Kinked tubing, blocked trap, or partially blocked line Trace the tubing for kinks; replace the water trap first, then the sampling line if needed
No waveform, display shows "---" Patient not connected yet, loose connection, or trap issue Check every connection from the module out to the patient
EtCO₂ reading lower than ABG PaCO₂ suggests O₂ compensation not activated on a high-FiO₂ patient; small leak somewhere Turn on O₂ compensation in CO₂ Setup; check all connections
🏥 Standard-Assumption Review Approach This module uses standard manufacturer, literature, and common ICU practice assumptions unless Dana or the reviewing team identifies a Thompson-specific exception. Reviewers should flag items that would be inaccurate or meaningfully different from current practice; exact part numbers, policy citations, and local wording do not need to block learner education.
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📋 Clinical Scenario — Think First
It's 0215. You're 4 minutes into a code on a 68-year-old patient in PEA. The LIFEPAK 15 shows EtCO₂ at 8 mmHg with a faint, irregular waveform. What's your first priority?
What would you do?

Module 4: EtCO₂ During CPR & Resuscitation AHA 2020

Why EtCO₂ Matters in a Code

During a code, you're making fast decisions with limited information. EtCO₂ is one of the few real-time signals that can tell you whether your compressions are actually moving blood — before a pulse check, before a blood gas, before anything else.

During cardiac arrest, CO₂ continues to be produced by cells — but it can only reach the lungs if blood is moving. EtCO₂ therefore directly reflects cardiac output and pulmonary blood flow during CPR. The better the compressions, the higher the EtCO₂.

🔑 Core Concept EtCO₂ = a real-time, non-invasive window into how effectively you are perfusing the patient. Higher EtCO₂ = better cardiac output from your compressions. Low EtCO₂ = inadequate perfusion.
>20
Target EtCO₂ during CPR (mmHg) — AHA Goal
<10
EtCO₂ after 20 min CPR: strong predictor of non-survival
≥35–40
Sudden rise = likely ROSC

Using EtCO₂ to Assess CPR Quality

The AHA and ERC recommend using EtCO₂ to provide real-time feedback on the effectiveness of chest compressions. Research consistently demonstrates that EtCO₂ correlates with the quality of cardiac output generated by CPR.

  • If EtCO₂ is below 10 mmHg during CPR, compression quality is inadequate — push harder, faster, allow full recoil, and minimize interruptions.
  • If EtCO₂ is 10–20 mmHg, compressions are marginal — reassess technique, rotate compressor, and consider whether reversible causes are being addressed.
  • If EtCO₂ is >20 mmHg, compressions are generating meaningful cardiac output.
📋 Clinical Scenario — CPR Quality Feedback
Your team is 8 minutes into a resuscitation for a patient in pulseless electrical activity (PEA). EtCO₂ on the LIFEPAK 15 reads 7 mmHg. The waveform shows a very shallow, irregular tracing. What does this tell you?
Interpretation: EtCO₂ of 7 mmHg indicates critically poor pulmonary blood flow. Either compressions are inadequate, or there is a reversible cause (hypovolemia, tension pneumothorax, tamponade, PE) significantly limiting cardiac output. This is a prompt to: check and improve compression depth/rate, rotate compressor immediately, and rapidly reassess for reversible causes.

Recognizing Return of Spontaneous Circulation (ROSC)

One of the most valuable uses of continuous EtCO₂ during a code is the early, non-invasive detection of ROSC before compressions are paused for a pulse check.

✅ ROSC Recognition A sudden, sustained rise in EtCO₂ — typically jumping from CPR-level values (10–20 mmHg) to 35 mmHg or higher — is a reliable indicator that the heart has resumed pumping spontaneously. This often occurs before any other detectable clinical sign.
35 15 0 CPR — Low EtCO₂ ↑ ROSC — Sudden rise
EtCO₂ waveform during CPR showing sudden rise at ROSC (green = post-ROSC)
🔎 Quick Check — Pause and retrieve
Your team is 9 minutes into a resuscitation. EtCO₂ has been steady at 18 mmHg. Suddenly it jumps to 42 mmHg. Compressions are still in progress. What do you call?
Call ROSC — that sudden, sustained rise to 35+ mmHg while compressions are ongoing is the classic EtCO₂ signature of spontaneous circulation returning. Stop compressions and check for a pulse. This is often the first sign before any other clinical indicator.

EtCO₂ as a Prognostic Indicator

Research from Ahrens et al. (2001) in a landmark multi-hospital study of 127 cardiac arrest patients found:

  • Patients with EtCO₂ persistently less than 10 mmHg throughout resuscitation had near-universal non-survival; survival to hospital discharge was rare when EtCO₂ remained below 10 mmHg at 20 minutes.
  • Patients with EtCO₂ greater than 20 mmHg had an 87% immediate resuscitation survival rate.
  • Patients surviving to discharge had significantly higher EtCO₂ values at all time points than non-survivors.
⚠️ Limitations & Important Caveats
  • Epinephrine: May cause a transient, small decrease in EtCO₂ values due to pulmonary vasoconstriction — do not misinterpret this as worsening CPR quality.
  • Sodium Bicarbonate: Administration increases CO₂ production and will cause EtCO₂ to rise — this rise does not indicate ROSC. Wait ≥5 minutes after bicarb before using EtCO₂ as a prognostic indicator.
  • EtCO₂ alone should not be the only criterion for terminating resuscitative efforts — clinical judgment, rhythm, duration, and reversible causes must all be considered.

The CPR Coach — An Emerging Role Worth Considering

A growing body of evidence supports adding a dedicated quality CPR coach to resuscitation teams. McDermott et al. (2025) describe the coach as a team member whose sole job during a code is to give real-time, verbal feedback to the compressor: rate, depth, recoil, switch timing, and pause length. That verbal loop offloads cognitive work from the team leader, who is already juggling rhythm analysis, medication timing, differential diagnosis, and family communication.

The role is not dependent on any specific device — a coach who is watching the compressor and listening to the timer adds value with or without technology. Reported improvements in CPR quality metric adherence are most pronounced when a coach is paired with real-time feedback (audio or visual) from the defibrillator, but the coach role by itself has been associated with tighter rate control, better compression fractions, and shorter peri-shock pauses.

This is presented here as an evidence-based practice for your team and code committee to consider — it is not yet a formal role at Thompson Health. If your unit is interested, the coach concept is easy to pilot: assign one experienced nurse at each code to stand at the head or shoulders of the patient, say nothing except compression feedback, and debrief afterward on what changed.

📊 AHA CPR Quality Targets
  • Compression rate: 100–120 per minute
  • Compression depth: ≥2 inches (5 cm) in adults
  • Complete chest recoil — no leaning
  • Chest compression fraction (CCF): ≥60% (expert target: ≥80%)
  • EtCO₂: >20 mmHg during CPR; goal as close to 25 mmHg as possible
  • Arterial diastolic BP >25–30 mmHg if arterial line in place
📋 Clinical Scenario — Think First
Your patient just achieved ROSC after 14 minutes of CPR. They're intubated. The ventilator is set at a rate of 20 and the EtCO₂ is reading 28 mmHg. What does this tell you?
What would you do?
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Module 5: EtCO₂ in Post-Resuscitation Care

The Post-ROSC Period: Why Ventilation Matters

ROSC is not the finish line. What happens to ventilation in the first hour post-resuscitation significantly affects neurological outcomes. EtCO₂ gives you continuous, non-invasive guidance on whether the patient is being ventilated to target.

Following return of spontaneous circulation (ROSC), the patient enters a critical physiological period. The brain — which suffered ischemia during arrest — is now uniquely vulnerable to secondary injury from abnormal CO₂ levels. EtCO₂ monitoring becomes an essential tool for protecting neurological outcomes.

35–45
Target EtCO₂ post-ROSC (mmHg)
Normocapnia goal
<35
Hypocapnia — causes cerebral vasoconstriction; avoid
>50
Hypercapnia — increases ICP, worsens outcomes; avoid

Avoiding Hypocapnia (Over-Ventilation)

Post-arrest hyperventilation is one of the most common — and most harmful — errors in post-resuscitation care. When CO₂ falls below 35 mmHg:

  • Cerebral blood vessels constrict, further reducing already-compromised cerebral blood flow
  • Tissue ischemia in the brain is worsened despite ROSC
  • Neurological outcomes are significantly worse

During the excitement and urgency of a post-code, bag-mask ventilation is frequently too fast. EtCO₂ monitoring provides immediate feedback to slow the ventilation rate before the ABG is even drawn.

⚠️ Post-Code Ventilation Rate Target 10 breaths per minute for adults post-arrest (unless contraindicated). Watch EtCO₂ continuously. If values are dropping below 35 mmHg, slow down ventilation immediately — do not wait for ABG results.

Avoiding Hypercapnia (Under-Ventilation)

Equally important is preventing CO₂ from rising excessively above 45–50 mmHg. Hypercapnia post-ROSC:

  • Increases intracranial pressure (ICP) due to cerebral vasodilation
  • Causes respiratory acidosis, worsening hemodynamic instability
  • May contribute to brain edema in the already-injured post-arrest brain

EtCO₂ and the PaCO₂–EtCO₂ Gradient Post-Arrest

Following cardiac arrest, pulmonary blood flow is often significantly disrupted. The gradient between arterial CO₂ (PaCO₂) and EtCO₂ may be wider than usual — sometimes 10–15 mmHg or more — due to V/Q mismatch from resuscitation-related lung injury, aspiration, or poor cardiac output.

🔬 Critical Practice Point Always obtain an arterial blood gas (ABG) soon after ROSC to establish the PaCO₂–EtCO₂ gradient for that patient. Once you know the patient's individual gradient, you can use EtCO₂ trending to continuously guide ventilator adjustments between ABGs. Do not rely solely on EtCO₂ in isolation post-arrest.

Targeted Temperature Management (TTM)

For patients undergoing TTM (targeted temperature management / therapeutic hypothermia), the relationship between EtCO₂ and PaCO₂ may be further altered by the effects of cooling on CO₂ solubility. During hypothermia, CO₂ becomes more soluble in blood, and measured PaCO₂ values depend on whether they are corrected for temperature (alpha-stat vs. pH-stat management). For this module, teach standard post-arrest normocapnia unless an active order set or provider direction specifies a different target; correlate EtCO₂ with ABG results because temperature management and V/Q changes can alter the patient's PaCO₂–EtCO₂ gradient.

Recognizing Re-Arrest

EtCO₂ monitoring provides early warning of hemodynamic deterioration and re-arrest. After ROSC, a patient's EtCO₂ should be in the 35–45 mmHg range. If EtCO₂ suddenly and significantly drops:

  • Back to CPR-level values (<20 mmHg): Immediately assess for pulse — re-arrest may have occurred.
  • Progressive decline: Assess for worsening cardiac output, tension pneumothorax (post-CPR), hemodynamic instability, or pulmonary embolism.

Integration with Post-Resuscitation Care Bundle

EtCO₂ monitoring is one component of a comprehensive post-ROSC bundle. Key concurrent priorities:

ParameterTargetRationale
EtCO₂ / PaCO₂35–45 mmHg (normocapnia)Optimize cerebral perfusion; avoid secondary brain injury
SpO₂ / PaO₂SpO₂ 94–98%; avoid hyperoxiaPrevent oxidative injury to ischemic brain
MAPAt least 65–70 mmHg unless provider or protocol specifies a different targetEnsure adequate cerebral perfusion pressure
TemperaturePer TTM protocol (32–36°C or normothermia)Neuroprotection; limit secondary injury
Glucose140–180 mg/dL (avoid extremes)Prevent hypo- and hyperglycemia-related brain injury
12-lead ECG / PCI-Capable TransferSTEMI or suspected coronary occlusion → activate transfer to Strong or another PCI-capable center for emergent angiographyTreat underlying coronary cause
📋 Clinical Scenario — Post-ROSC Ventilation
A 58-year-old male achieves ROSC after 14 minutes of CPR for VF arrest. He remains intubated and unresponsive. Post-ROSC EtCO₂ is 22 mmHg. The nurse practitioner is preparing for transfer to Strong for PCI-capable care. The bedside nurse notes she is bagging the patient at approximately 20 breaths per minute.
Problem: EtCO₂ of 22 mmHg indicates the patient is being hyperventilated (over-ventilation has lowered CO₂). At 20 breaths/min, cerebral vasospasm and reduced CBF are occurring at a time when the brain most needs perfusion.

Intervention: Immediately slow the ventilation rate to 10 breaths/min. Recheck EtCO₂ within 2–3 breaths. Target 35–45 mmHg. Obtain ABG at first opportunity to confirm PaCO₂ and calculate gradient. Notify team of concern.
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Module 6: EtCO₂ on the Stryker LIFEPAK 15 Device-Specific

📋 Source Content in this module is based on the LIFEPAK 15 Monitor/Defibrillator Operating Instructions (©2019 Physio-Control, Inc./Stryker, Document 3314911-030) and the official EtCO₂ Performance Evaluation checklist (GDR 3301872_B). Always refer to the most current operating instructions for your specific device.

How the LIFEPAK 15 Measures EtCO₂

The LIFEPAK 15 uses Microstream® non-dispersive infrared (NDIR) spectroscopy — a sidestream capnography technology. The CO₂ FilterLine set draws a gas sample from the patient at 50 mL/min through small-bore tubing into the device's internal CO₂ sensor. Key technical features:

  • Micro-sample capture: 15 microliters — allows fast rise time and accurate readings even at high respiratory rates
  • Low sampling flow minimizes fluid/secretion accumulation and maintains waveform shape
  • Proprietary IR source emits only CO₂-specific wavelengths — no compensation needed for O₂, anesthetic agents, or water vapor
  • BTPS (Body Temperature Pressure Saturated) correction available via Setup: 0.97 × measured EtCO₂
  • Initialization and warm-up: typically <30 seconds, may take up to 2.5 minutes

EtCO₂ Monitoring Procedure — Step by Step

These steps are here as a reference. Focus on understanding when and why to use the device — the step-by-step guide is available any time you need it.
  1. Press ON
    Power on the LIFEPAK 15. The device will begin its startup self-test sequence.
  2. Select the appropriate FilterLine® for your patient
    • Intubated patient: Use an intubated FilterLine (connects to ETT adapter)
    • Non-intubated patient: Use an oral-nasal or nasal cannula FilterLine set
    Select the correct device for accurate sampling — do not interchange FilterLine types.
  3. Open the CO₂ port door on the LIFEPAK 15
    The CO₂ port door is located on the device. A broken or missing port door may allow liquid contamination of the internal sensor — report any damage to biomedical engineering.
  4. Insert the FilterLine connector; turn clockwise until tight
    A loose connection will cause falsely low EtCO₂ values while still displaying a waveform — a potentially dangerous scenario. Always ensure the connector is firmly seated and tight. Tip: hand-straighten the tubing after removing from the package before connecting — this reduces the likelihood of the connection loosening during use.
  5. Verify the CO₂ area is displayed on the screen
    The EtCO₂ monitor activates automatically when it senses the FilterLine connection. Note the CO₂ INITIALIZING self-test screen message — this is normal. Wait for initialization to complete before connecting to the patient.
  6. Display the CO₂ waveform in Channel 2 or 3
    Use the SPEED DIAL to highlight Channel 2 (or 3) and select the CO₂ waveform. The waveform displays at 12.5 mm/sec (compressed) on screen; printouts are at 25 mm/sec.
  7. Connect the FilterLine set to the patient
    • Intubated: Connect the FilterLine adapter to the ETT Y-piece or swivel adapter
    • Non-intubated: Place oral-nasal cannula with sample prongs in nares and oral port near mouth
    Route the tubing carefully to minimize pull on the patient's airway.
  8. Confirm EtCO₂ value and waveform are displayed
    The monitor automatically selects the scale for best waveform visualization. A CO₂ value will appear once CO₂ concentration exceeds 3.5 mmHg. The monitor will begin displaying respiratory rate once valid breaths (>8 mmHg) are detected — averaged over the last 8 breaths.
  9. Adjust scale if desired (optional)
    Use the SPEED DIAL to highlight the CO₂ area and select desired scale:
    • Autoscale (default)  |  0–20 mmHg  |  0–50 mmHg  |  0–100 mmHg
    Standard ICU use: Autoscale or 0–50 mmHg is typically appropriate.

Alarm Types on the LIFEPAK 15

AlarmAdjustable?Trigger ConditionAction
EtCO₂ HighYes — via ALARMS buttonEtCO₂ exceeds set high limitAssess patient; consider hypoventilation, obstruction
EtCO₂ LowYes — via ALARMS buttonEtCO₂ falls below set low limitAssess patient; consider hyperventilation, decreasing CO
No Breath / Alarm ApneaNo — automaticNo CO₂ >8 mmHg for 30 secondsAssess patient immediately — check airway, breathing
FiCO₂ (Inspired CO₂)No — automaticInspired CO₂ above thresholdCheck for CO₂ rebreathing; check circuit
⚠️ Note on Alarm Apnea vs. No Breath Some LIFEPAK 15 software versions display "ALARM APNEA" while others display "ALARM NO BREATH." These messages are equivalent. Both indicate that no breath with CO₂ >8 mmHg has been detected for 30 seconds — treat as an urgent patient safety event.

When No CO₂ Is Detected During Cardiac Arrest

If the waveform shows dashes "- - -" or a flat line at or near zero during a resuscitation, rapidly evaluate these causes in order:

CategoryPossible Causes
Equipment FilterLine disconnected from ETT  |  Loose FilterLine at device port  |  System purging (ET medication administration)  |  Auto-zeroing in progress  |  System resetting after shock delivery
Airway Esophageal intubation or ETT dislodgment  |  ETT obstruction (secretions, kinking, cuff herniation)
Physiological Inadequate CPR generating no pulmonary blood flow  |  Apnea  |  Massive pulmonary embolism  |  Exsanguination

Troubleshooting Common LIFEPAK 15 EtCO₂ Issues

Screen Message / ObservationPossible CauseCorrective Action
ALARM NO BREATH — waveform flat/zero No breath for 30 sec; loose FilterLine; patient disconnected Check patient first; then check/tighten FilterLine connection
CO₂ FILTERLINE OFF — waveform "- - -" FilterLine not connected or not secure Connect FilterLine; turn clockwise until tight and firmly seated
CO₂ FILTERLINE PURGING — waveform "- - -" Fluid in line, kink, or rapid altitude change Disconnect then reconnect FilterLine; may need to replace FilterLine
CO₂ FILTERLINE BLOCKAGE — waveform "- - -" FilterLine kinked or clogged with fluid/secretions Disconnect, reconnect, and change the FilterLine set
CO₂ INITIALIZING — waveform "- - -" Normal initialization after FilterLine connected Wait for initialization to complete (up to 2.5 min)
AUTO ZEROING — waveform "- - -" Normal self-maintenance routine (hourly, after shock, temp/pressure change) No action required; system resets automatically within ~20 sec after shock
EtCO₂ values erratic Loose connection; leak in FilterLine; patient spontaneously breathing against ventilator Check and tighten all connections; check for line leaks; if patient breathing spontaneously, no action needed
EtCO₂ consistently lower than expected Loose FilterLine at device; hyperventilation; physiological cause (e.g., PE) Check connection; reduce ventilation rate; correlate with clinical assessment and ABG
EtCO₂ consistently higher than expected Hypoventilation; COPD/chronic CO₂ retention; inadequate ventilation rate Increase ventilatory rate/volume; notify provider; check ventilator settings
XXX instead of EtCO₂ value CO₂ module malfunction Turn device off then on; if persists, contact Biomedical Engineering
🔑 LIFEPAK 15 Key Reminders
  • FilterLine sets are single-patient use only — do not clean or reuse
  • The monitor shows the maximum CO₂ over the last 20 seconds — falling values may take up to 20 sec to reflect on the display
  • CO₂ must be >3.5 mmHg for a numeric value to appear; must be >8 mmHg to count as a valid breath for RR calculation
  • Never use the EtCO₂ monitor as a standalone diagnostic apnea monitor — it is an adjunct to clinical assessment
  • If the CO₂ port door is broken or missing — tag device out of service and notify Biomedical Engineering

📝 Knowledge Assessment

Answer all 12 questions, then select Submit Assessment. A score of 80% or higher (10/12) is required to complete this module. You must answer every question before submitting.

💡 Tip Review the rationale for each question after submission to reinforce learning — even for questions you answered correctly.

1. What is the normal range for end-tidal CO₂ (EtCO₂) in a spontaneously breathing adult with normal cardiopulmonary function?

✅ Correct. The normal EtCO₂ range is 35–45 mmHg, reflecting normal alveolar ventilation. Under normal V/Q matching, EtCO₂ approximates PaCO₂ with a gradient of only 1–5 mmHg.
❌ Incorrect. The normal EtCO₂ range is 35–45 mmHg. Values outside this range indicate either hypoventilation (above 45 mmHg) or hyperventilation/poor perfusion (below 35 mmHg).

2. During cardiac arrest with CPR in progress, what does a low EtCO₂ value (<10 mmHg) primarily indicate?

✅ Correct. During CPR, EtCO₂ directly reflects cardiac output and pulmonary blood flow. Low values (<10 mmHg) indicate that compressions are not generating adequate blood flow to carry CO₂ to the lungs. This is a signal to improve compression quality.
❌ Incorrect. During CPR, EtCO₂ is a surrogate for cardiac output. A low value (<10 mmHg) means compressions are not generating sufficient pulmonary blood flow — not a ventilation or metabolic issue.

3. According to AHA guidelines, what is the EtCO₂ target during high-quality CPR?

✅ Correct. The AHA recommends targeting EtCO₂ >20 mmHg during CPR, with the ideal goal being as close to 25 mmHg as possible. Values <10 mmHg after 20 minutes of CPR are associated with near-universal non-survival.
❌ Incorrect. The AHA CPR quality target for EtCO₂ is >20 mmHg (ideally approaching 25 mmHg). This threshold reflects meaningful cardiac output being generated by chest compressions.

4. During a resuscitation, EtCO₂ abruptly rises from 14 mmHg to 42 mmHg. What does this most likely indicate?

✅ Correct. A sudden, sustained rise in EtCO₂ to ≥35 mmHg during CPR is a hallmark sign of ROSC. The resumption of spontaneous cardiac output dramatically increases pulmonary blood flow, allowing CO₂ to be expelled — often before any other clinical sign of ROSC is detectable.
❌ Incorrect. A sudden rise from CPR-level EtCO₂ (~14 mmHg) to a near-normal value (~42 mmHg) is the classic pattern of ROSC. A disconnection would cause a sudden drop to zero; bicarb would cause a moderate rise but not typically this magnitude.

5. Which phase of the capnography waveform represents the actual EtCO₂ value recorded by the monitor?

✅ Correct. Point D — the peak of Phase III at the very end of exhalation — is where alveolar gas (and therefore CO₂ concentration) is at its maximum. This is the EtCO₂ value captured and displayed by the monitor.
❌ Incorrect. The EtCO₂ value is recorded at Point D — the peak of the alveolar plateau at the very end of exhalation — where the gas most closely represents alveolar (and arterial) CO₂ concentration.

6. A patient on a continuous IV opioid infusion has SpO₂ of 98% on 2L nasal cannula. The EtCO₂ monitor reads 58 mmHg with an abnormal waveform. What is the correct interpretation?

✅ Correct. This is a classic OIRD scenario. Supplemental oxygen maintains SpO₂ despite significant hypoventilation — SpO₂ is a late indicator. The EtCO₂ of 58 mmHg signals dangerous hypercapnia from opioid-induced respiratory depression. Assess the patient immediately, stimulate, reduce opioid if safe, and notify the provider. This is exactly why capnography is superior to SpO₂ for detecting OIRD.
❌ Incorrect. This scenario illustrates a critical limitation of pulse oximetry: supplemental oxygen can maintain SpO₂ even when the patient is dangerously hypoventilating. An EtCO₂ of 58 mmHg represents significant CO₂ retention and OIRD — assess the patient immediately.

7. What is the recommended EtCO₂ target for a mechanically ventilated patient immediately following ROSC from cardiac arrest?

✅ Correct. Post-ROSC, the goal is normocapnia (EtCO₂ 35–45 mmHg). Hypocapnia causes cerebral vasoconstriction and worsens neurological outcomes. Hypercapnia increases ICP and causes respiratory acidosis. Both extremes must be avoided.
❌ Incorrect. The target post-ROSC is normocapnia: EtCO₂ 35–45 mmHg. Hypocapnia (<35 mmHg) causes cerebral vasoconstriction and secondary brain injury. This is one of the most clinically important applications of continuous capnography in post-arrest care.

8. The capnography waveform shows an upward-sloping alveolar plateau that resembles a "shark fin." What is the most likely clinical cause?

✅ Correct. The "shark fin" pattern (upward-sloping expiratory plateau) indicates uneven alveolar emptying due to airflow obstruction. Bronchospasm, asthma, COPD exacerbation, and partial ETT kinking are the most common causes. Assess for wheezing and consider bronchodilator therapy.
❌ Incorrect. The shark fin waveform — upward-sloping Phase III — indicates airflow obstruction causing uneven alveolar emptying. Bronchospasm and COPD are classic causes. Rebreathing causes baseline elevation; esophageal intubation causes no waveform; hyperventilation causes low numerical values.

9. On the LIFEPAK 15, which of the following EtCO₂ alarms is automatic and cannot be adjusted by the nurse?

✅ Correct. The No Breath (also displayed as "Alarm Apnea" on some LIFEPAK 15 software versions) alarm is automatic and not adjustable. It activates when no breath with CO₂ >8 mmHg is detected for 30 consecutive seconds. The FiCO₂ alarm is also automatic and not adjustable. The EtCO₂ High and Low alarms are adjustable via the ALARMS button.
❌ Incorrect. The No Breath alarm (and FiCO₂ alarm) on the LIFEPAK 15 are automatic and not adjustable. They trigger based on fixed physiological thresholds. The EtCO₂ High and Low alarms are adjustable via the ALARMS button.

10. You are setting up EtCO₂ monitoring on the LIFEPAK 15 for an intubated patient. After connecting the FilterLine, the monitor displays "CO₂ INITIALIZING" and the waveform shows "- - -". What should you do?

✅ Correct. CO₂ INITIALIZING is a normal startup message indicating the EtCO₂ module is completing its self-test and warm-up sequence. This typically completes within 30 seconds but may take up to 2.5 minutes. No action is needed — wait for initialization to complete before connecting to the patient.
❌ Incorrect. "CO₂ INITIALIZING" is a normal startup message. The EtCO₂ module is performing its self-test and warm-up — this is expected behavior when a FilterLine is first connected. Wait up to 2.5 minutes for completion before troubleshooting.

11. A patient receiving sodium bicarbonate during cardiac resuscitation has a sudden rise in EtCO₂ from 12 mmHg to 28 mmHg. You should:

✅ Correct. Sodium bicarbonate administration causes CO₂ production to increase as bicarbonate is converted to CO₂ and water, which can transiently elevate EtCO₂. A rise from 12 to 28 mmHg — while significant — does not reach the typically expected ROSC level (>35 mmHg). Always correlate with pulse check, waveform quality, and other clinical signs. Do not stop CPR based on EtCO₂ alone after bicarb administration.
❌ Incorrect. Sodium bicarbonate causes a transient rise in EtCO₂ due to CO₂ generation — this can mimic ROSC. Always correlate with a pulse check and other clinical signs before stopping CPR. A true ROSC typically causes EtCO₂ to rise above 35 mmHg and sustain.

12. During continuous EtCO₂ monitoring of a ventilated patient post-ROSC, you notice the EtCO₂ has gradually declined from 42 mmHg to 18 mmHg over the past 20 minutes. The SpO₂ is still 96%. What is your priority action?

✅ Correct. A decline in EtCO₂ from 42 to 18 mmHg in a post-ROSC patient is a critical alarm — this pattern suggests decreasing cardiac output, possible re-arrest, PE, worsening hemodynamic instability, or airway compromise. SpO₂ lags behind and will not fall until oxygenation is compromised. Assess the patient immediately, check for pulse, and notify the provider urgently. The PaCO₂–EtCO₂ gradient must also be reconsidered — obtain an ABG.
❌ Incorrect. A progressive fall in EtCO₂ from 42 to 18 mmHg in a post-ROSC patient is a critical deterioration signal. This may indicate re-arrest, hemodynamic collapse, PE, or airway compromise. SpO₂ lags significantly — do not be falsely reassured. Assess the patient immediately.
—
out of 12 questions correct

References

  1. Ahrens T, Schallom L, Bettorf K, et al. End-tidal carbon dioxide measurements as a prognostic indicator of outcome in cardiac arrest. Am J Crit Care. 2001;10(6):391–398.
  2. Carlisle H. Promoting the use of capnography in acute care settings: an evidence-based practice project. J Perianesth Nurs. 2015;30(3):201–208.
  3. McDermott KL, Rajzer-Wakeham KL, Andres JM, et al. Impact of a quality cardiopulmonary resuscitation coach on pediatric intensive care unit resuscitation teams. Am J Crit Care. 2025;34(1):21–29.
  4. Pignatiello GA. Discussion guide for the McDermott article. Am J Crit Care. 2025;34(1):30–31.
  5. Setälä PA, Virkkunen IT, Kämäräinen AJ, et al. End-tidal carbon dioxide output in manual cardiopulmonary resuscitation versus active compression-decompression device during prehospital quality controlled resuscitation: a case series study. Emerg Med J. 2018;35(7):428–433.
  6. St. John RE. End-tidal carbon dioxide monitoring. Crit Care Nurse. 2003;23(4):83–88.
  7. Physio-Control, Inc./Stryker. LIFEPAK® 15 Monitor/Defibrillator Operating Instructions. Document 3314911-030. Redmond, WA: Physio-Control; 2019.
  8. Physio-Control, Inc./Stryker. EtCO₂ Performance Evaluation Checklist — LIFEPAK 15. GDR 3301872_B. 2018.
  9. American Heart Association. 2020 American Heart Association Guidelines for CPR and Emergency Cardiovascular Care. Dallas, TX: AHA; 2020.
  10. GE Healthcare. E-miniC CO₂ Airway Module — Product Specification Sheet. Document DOC2030693 Rev 1. Helsinki, Finland: GE Healthcare Finland Oy; 2017.
  11. GE Healthcare. CARESCAPE Monitor B650 — Clinical Reference Guide. Helsinki, Finland: GE Healthcare Finland Oy.