CAPNOGRAPHY: THE VENTILATION VITAL SIGN Mazen Kherallah, MD FCCP Critical 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 + Glucose energy CO 2 blood lungs CO 2 breath CO 2 Respiratory Cycle

METABOLISM PERFUSIONVENTILATION 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   CO2Hypoventilation Physiology

Why ETCO2 I Have my Pulse Ox?  Oxygen Saturation  Reflects Oxygenation  SpO2 changes lag when patient is hypoventilating or apneic  Should be used with Capnography  Carbon Dioxide  Reflects Ventilation  Hypoventilation/Apnea detected immediately  Should be used with pulse Oximetry Pulse OximetryCapnography

What does it really do for me?  Bronchospasms: Asthma, COPD, Anaphlyaxis  Hypoventilation: Drugs, Stroke, CHF, Post-Ictal  Shock & Circulatory compromise  Hyperventilation Syndrome: Biofeedback  Verification of ETT placement  ETT surveillance during transport  Control ventilations during CHI and increased ICP  CPR: compression efficacy, early signs of ROSC, survival predictor Non-Intubated ApplicationsIntubated Applications

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

PaCO 2 -PetCO 2 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  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  ETCO 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  ETCO 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 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 J Int Care Med, 12(1): 18-32, 1997

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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