CAPNOGRAPHY: THE VENTILATION VITAL SIGNMazen Kherallah, MD FCCPCritical Care Medicine and Infectious DIsease

Objectives

Define Capnography Discuss Respiratory Cycle Discuss ways to collect ETCO2

information Discuss Non-intubated vs. intubated

patient uses Discuss different waveforms and

treatments of them.

So what is Capnograhy?

Capnography- Continuous analysis and recording of Carbon Dioxide concentrations in respiratory gases ( I.E. waveforms and numbers)

Capnometry- Analysis only of the gases no waveforms

Respiratory Cycle

Breathing- Process of moving oxygen into the body and CO2 out can be passive or non-passive.

Metabolism-Process by which an organism obtains energy by reacting O2 with glucose to obtain energy. Aerobic- glucose+O2 = water vapor, carbon

dioxide, energy (2380 kJ) Anaerobic- glucose= alcohol, carbon

dioxide, water vapor, energy (118 kJ)

Respiratory Cycle con’t

Ventilation- Rate that gases enters and leaves the lungs Minute ventilation- Total volume of gas

entering lungs per minute Alveolar Ventilation- Volume of gas that

reaches the alveoli Dead Space Ventilation- Volume of gas that

does not reach the respiratory portions ( 150 ml)

Oxygen -> lungs -> alveoli -> blood

muscles + organs

Oxygen

cells

Oxygen

Oxygen +Glucose

energy

CO2

blood

lungs

CO2

breath

CO2

Respiratory Cycle

METABOLISM PERFUSION VENTILATION

ALL THREE ARE IMPORTANT!

Respiratory Cycle

How is ETCO2 Measured?

Semi-quantitative capnometry Quantitative capnometry Wave-form capnography

Semi-Quantitative Capnometry Relies on pH change Paper changes color

Purple to Brown to Yellow

Quantitative Capnometry

Absorption of infra-red

light Gas source

Side Stream In-Line

Factors in choosing device:

Warm up time Cost Portability

Waveform Capnometry

Adds continuous waveform display to the ETCO2 value. Additional information in waveform shape can provide clues about causes of poor oxygenation.

Interpretation of ETCO2

Excellent correlation between ETCO2 and cardiac output when cardiac output is low.

When cardiac output is near normal, then ETCO2 correlates with minute volume.

Only need to ventilate as often as a “load” of CO2 molecules are delivered to the lungs and exchanged for 02 molecules

Hyperventilation Kills

EtCO2 Values

Normal 35 – 45 mmHg Hypoventilation > 45 mmHg Hyperventilation < 35 mmHg

Relationship between CO2 and RR RR CO2 Hyperventilation RR CO2 Hypoventilation

Physiology

Why ETCO2 I Have my Pulse Ox?

Oxygen SaturationReflects OxygenationSpO2 changes lag when patient is hypoventilating or apneicShould be used with Capnography

Carbon Dioxide

Reflects Ventilation

Hypoventilation/Apnea detected immediately

Should be used with pulse Oximetry

Pulse Oximetry Capnography

What does it really do for me?

Bronchospasms: Asthma, COPD, AnaphlyaxisHypoventilation: Drugs, Stroke, CHF, Post-IctalShock & Circulatory compromiseHyperventilation Syndrome: Biofeedback

Verification of ETT placementETT surveillance during transportControl ventilations during CHI and increased ICPCPR: compression efficacy, early signs of ROSC, survival predictor

Non-Intubated Applications Intubated Applications

NORMAL CAPNOGRAM

NORMAL CAPNOGRAM

Phase I is the beginning of exhalation Phase I represents most of the anatomical dead

space Phase II is where the alveolar gas begins to mix

with the dead space gas and the CO2 begins to rapidly rise

The anatomic dead space can be calculated using Phase I and II

Alveolar dead space can be calculated on the basis of : VD = VDanat + VDalv

Significant increase in the alveolar dead space signifies V/Q mismatch

NORMAL CAPNOGRAM

Phase III corresponds to the elimination of CO2 from the alveoli

Phase III usually has a slight increase in the slope as “slow” alveoli empty

The “slow” alveoli have a lower V/Q ratio and therefore have higher CO2 concentrations

In addition, diffusion of CO2 into the alveoli is greater during expiration. More pronounced in infants

ET CO2 is measured at the maximal point of Phase III.

Phase IV is the inspirational phase

ABNORMALITIES

Increased Phase III slope Obstructive lung

disease Phase III dip

Spontaneous resp Horizontal Phase III

with large ET-art CO2 change Pulmonary

embolism cardiac output Hypovolemia

Sudden in ETCO2 to 0 Dislodged tube Vent malfunction ET obstruction

Sudden in ETCO2 Partial obstruction Air leak

Exponential Severe

hyperventilation Cardiopulmonary

event

ABNORMALITIES

Gradual Hyperventilation Decreasing temp Gradual in

volume Sudden increase

in ETCO2 Sodium bicarb

administration Release of limb

tourniquet

Gradual increase Fever Hypoventilation

Increased baseline Rebreathing Exhausted CO2

absorber

PaCO2-PetCO2 gradient

Usually <6mm Hg PetCO2 is usually less Difference depends on the number of

underperfused alveoli Tend to mirror each other if the slope of

Phase III is horizontal or has a minimal slope Decreased cardiac output will increase the

gradient The gradient can be negative when healthy

lungs are ventilated with high TV and low rate Decreased FRC also gives a negative gradient

by increasing the number of slow alveoli

LIMITATIONS

Critically ill patients often have rapidly changing dead space and V/Q mismatch

Higher rates and smaller TV can increase the amount of dead space ventilation

High mean airway pressures and PEEP restrict alveolar perfusion, leading to falsely decreased readings

Low cardiac output will decrease the reading

USES

Metabolic Assess energy expenditure

Cardiovascular Monitor trend in cardiac output Can use as an indirect Fick method, but

actual numbers are hard to quantify Measure of effectiveness in CPR Diagnosis of pulmonary embolism: measure

gradient

PULMONARY USES

Effectiveness of therapy in bronchospasm Monitor PaCO2-PetCO2 gradient Worsening indicated by rising Phase III without

plateau Find optimal PEEP by following the gradient.

Should be lowest at optimal PEEP. Can predict successful extubation.

Dead space ratio to tidal volume ratio of >0.6 predicts failure. Normal is 0.33-0.45

Limited usefulness in weaning the vent when patient is unstable from cardiovascular or pulmonary standpoint

Confirm ET tube placement

Normal Wave Form

Square box waveform

ETCO2 35-45 mm Hg

Management: Monitor Patient

Dislodged ETT

Loss of waveform Loss of ETCO2

reading Management:

Replace ETT

Esophageal Intubation

Absence of waveform Absence of ETCO2 Management: Re-Intubate

CPR

Square box waveform ETCO2 10-15 mm Hg (possibly higher)

with adequate CPR Management: Change Rescuers if ETCO2

falls below 10 mm Hg

Obstructive Airway

Shark fin waveform With or without prolonged expiratory

phase Can be seen before actual attack Indicative of Bronchospasm( asthma,

COPD, allergic reaction)

ROSC (Return of Spontaneous Circulation) During CPR sudden increase of ETCO2

above 10-15 mm Hg Management: Check for pulse

Rising Baseline

Patient is re-breathing CO2 Management: Check equipment for

adequate oxygen flow If patient is intubated allow more time to

exhale

Hypoventilation

Prolonged waveform ETCO2 >45 mm Hg Management: Assist ventilations or

intubate as needed

Hyperventilation

Shortened waveform ETCO2 < 35 mm Hg Management: If conscious gives

biofeedback. If ventilating slow ventilations

Patient breathing around ETT Angled, sloping down stroke on the

waveform In adults may mean ruptured cuff or

tube too small In pediatrics tube too small Management: Assess patient,

Oxygenate, ventilate and possible re-intubation

Curare cleft

Curare Cleft is when a neuromuscular blockade wears off

The patient takes small breaths that causes the cleft

Management: Consider neuromuscular blockade re-administration

CAPNOGRAM #1

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CAPNOGRAM #2

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CAPNOGRAM #3

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CAPNOGRAM #5

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CAPNOGRAM #6

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CAPNOGRAM #8

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Now what does all this mean to me? ETCO2 is a great tool to help monitor the

patients breath to breath status. Can help recognize airway obstructions

before the patient has signs of attacks Helps you control the ETCO2 of head

injuries Can help to identify ROSC in cardiac

arrest