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) Respiratory Cycle Oxygen -> lungs -> alveoli -> blood Oxygen breath CO2 lungs muscles + organs Oxygen CO2 energy blood CO2 cells Oxygen + Glucose Respiratory Cycle ALL THREE ARE IMPORTANT! METABOLISM PERFUSION VENTILATION 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 Physiology Relationship between CO2 and RR RR CO2 RR CO2 Hyperventilation Hypoventilation Why ETCO2 I Have my Pulse Ox? Pulse Oximetry Capnography when patient is hypoventilating or apneic Should be used with Capnography detected immediately Should be used with pulse Oximetry Oxygen Saturation Reflects Oxygenation SpO2 changes lag Carbon Dioxide Reflects Ventilation Hypoventilation/Apnea What does it really do for me? Non-Intubated Applications Bronchospasms: Asthma, COPD, Anaphlyaxis Hypoventilation: Drugs, Stroke, CHF, Post-Ictal Shock & Circulatory compromise Hyperventilation Syndrome: Biofeedback Intubated Applications Verification of ETT placement ETT surveillance during transport Control ventilations during CHI and increased ICP CPR: compression efficacy, early signs of ROSC, survival predictor 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 Sudden in ETCO2 to 0 Dislodged tube Vent malfunction ET obstruction Phase III dip Spontaneous resp Horizontal Phase III with large ET-art CO2 change Pulmonary embolism cardiac output Hypovolemia Sudden in ETCO2 Partial obstruction Air leak Exponential Severe hyperventilation Cardiopulmonary event ABNORMALITIES Gradual Gradual increase Hyperventilation Fever Decreasing Hypoventilation temp Gradual in volume Sudden increase in ETCO2 Sodium bicarb administration Release of limb tourniquet Increased baseline Rebreathing Exhausted absorber CO2 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 1015 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 CAPNOGRAM #2 J Int Care Med, 12(1): 18-32, 1997 CAPNOGRAM #3 J Int Care Med, 12(1): 18-32, 1997 CAPNOGRAM #4 J Int Care Med, 12(1): 18-32, 1997 CAPNOGRAM #5 J Int Care Med, 12(1): 18-32, 1997 CAPNOGRAM #6 J Int Care Med, 12(1): 18-32, 1997 CAPNOGRAM #7 J Int Care Med, 12(1): 18-32, 1997 CAPNOGRAM #8 J Int Care Med, 12(1): 18-32, 1997 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