Capnography Edward C. Adlesic, DMD University of Pittsburgh School of Dental Medicine 2018 North Carolina Program Capnography non invasive monitor for ventilation measures end tidal CO2 early detection hyperventilation a hypoventilation airway obstruction a apnea correct ET tube placement early rise in CO2 during MH crisis Pulmonary Physiology Oxygenation 2 most vital functions of the pulmonary system delivery oxygen to lungs for aerobic cellular metabolism ( oxygenation ) ventilation to maintain appropriate oxygen & CO2 concentrations Oxygen is delivered to the lung Oxygen diffuses from alveoli into pulmonary capillaries dissolved in blood ( minor component ) bound to hemoglobin ( major component ) Used for aerobic metabolism in tissue Monitor with pulse oximetry and arterial blood gases 1
Pulse Oximetry Accurate monitor for arterial oxygen saturation a oxygenation No information on ventilation when using supplemental oxygen High FIO2 concentrations can maintain saturation even with inadequate ventilation while developing hypercarbia & acidosis FIO 2 a PaO 2 & P A O 2 Desaturation 6 physiologic and pathologic causes of desaturation FIO2 < 0.21 diffusion defect in alveoli barometric pressure < 760 mm right to left shunts low V/Q hypoventilation 2
Ventilation Definition: gas exchange between alveoli in lungs and external environment Oxygen diffuses into blood Carbon dioxide in mixed venous blood diffuses into alveoli and exhaled from lungs Alveolar Gas Partial Pressure Alveolar partial pressure of oxygen & carbon dioxide ( P AO2 & P ACO2 ) depends upon FIO2 concentration alveolar ventilation alveolar perfusion oxygen consumption carbon dioxide production by cells Decrease in respiratory rate or tidal volume ( V T ) or both normal tidal volume = 6 to 10 ml/kg Other factors for hypoventilation respiratory depression by medications airway obstruction V/Q mismatch increased alveolar dead space 3
PaO 2 & P A O 2 will decrease unless you h FIO 2 ( temporary fix ) will eventually decrease P ACO2 & P aco2 will increase Awake patients for every 1 mm h in P ACO2 a h ventilation by 2 L/min As CO2 levels increase, ventilations increase Pulse Oximetry & Can pulse ox monitor ventilation? Room air + hypoventilation results in exaggerated decrease in the volume of O 2 in the lungs create imbalance between O 2 delivered to alveoli & amount diffusing into blood get concentration of N 2 and CO 2 in alveoli that causes additional in alveolar O 2 Pulse Ox & Drop in P A O 2 & SpO2 is greater than the h P A CO 2 Chest 2004 study oxygen dropped 30 mm CO 2 increased only 5 mm pulse ox detected changes before capnograph on room air 4
FIO 2 = 0.21 ( Room Air ) P ACO2 > 65 mm results in P AO2 < 60 mm SpO 2 < 90% On room air can not hypoventilate to P ACO2 > 70 mm without SpO 2 < 90% Precludes the risk of CO2 narcosis & apnea using a pulse oximeter Supplemental Oxygen & don t concentrate N 2 and CO 2 in alveoli deliver higher FIO 2 to alveoli P A O 2 drops less a P a O 2 drops less Pulse ox readings will not supplemental oxygen 30% ( FIO2 =.30 ) as P A CO 2 rises to 90 P A O 2 only drops to 100 Pulse ox will still read ~ 98 to 100 Oxygen Delivery Systems Case Report Nasal cannula FIO 2 = 20 + ( 4 X Liters per min O 2 ) 1.0 L / min = 24% 2.0 L /min = 28% 3.0 L / min = 32% 4.0 L / min = 36% 6.0 L / min = 44% GI endoscopy with patient controlled morphine anesthesia ( PCA ) & high flow face mask oxygen Pulse ox read 92 to 95 during the case, but the patient became non responsive Blood gas ph = 7.02 PaCO 2 = 102 Patient developed carbon dioxide narcosis Chest 2004: 126; 1552 5
Case Report #2 Case Report #2 75 y.o. with femur fx gets hip replacement PACU: ET tube, 100% O2, spontaneous breathing, shallow breathing SpO2 94 to 96 Becomes unresponsive; narcan no change; continues for 3.5 hr ABG: PaO2 = 213, PaCO2 = 265, ph = 6.65 Diagnosis: alveolar hypoventilation hypercarbia but well oxygenated probably secondary to post op analgesics + anesthetic agents h P ACO2 will h ventilation but excessive elevations of CO2 will centrally depress ventilation monitoring with capnography prevents this Mayo Clin Proc. 1998; 73: 51 Conclusions Pulse oximetry can detect hypoventilation when breathing room air patient can not reach CO 2 levels > 70 without the pulse ox dropping to 90 or less Open airway technique can correct arterial hypoxia ( SpO2 < 90 ) by increasing the FIO2 but risk of undetected hypercarbia which can if left untreated cause narcosis and apnea Conclusions If you use supplemental oxygen especially with deep sedation, the pulse ox will not detect hypoventilation capnography is necessary Reasonable to apply this to moderate sedation as well Chest. 2004: 126; 1552 6
Monitoring Ventilation with Capnography Physiology of Ventilation at end of inspiration airway & lungs are filled with CO2 free gas CO2 diffuses from blood into the lungs concentration depends upon alveolar V/Q alveoli with high V/Q will have less CO2 diluted by O2 most exhaled during early Phase II alveoli with low V/Q will have high CO2 minor O2 dilution exhaled during late Phase III Mainstream Capnograph CO2 sampling sensor is attached directly to the ET tube IR sensor no gas sampling back to monitor sensors are heated to 40 0 C to eliminate water vapor faster response time than sidestream sensor is hot & can burn the patient Sidestream Capnograph CO2 sensor is in the monitor pump aspirates a gas sample to unit optimal rate a 50 to 200 ml/min sample size exceeds expired gas flow contaminate sample a PETCO2 i delay of 1 to 4 seconds to see PETCO2 waveform & number can use on intubated & nonintubated tracing is more rounded than mainstream 7
Time Capnogram Time Capnogram Phase I starts at end of inspiratory phase 0 little to no CO2 in external air PCO2 = 0 Internet images beginning of expiratory phase a PCO2 still is 0 anatomical dead space ( 150 ml of space ) not involved in gas exchange Time Capnography Time Capnogram Phase II CO2 from alveoli mix with dead space see a sharp rise in PETCO2 expiratory flow is very rapid in Phase II Alveoli Phase III CO2 rich alveolar gas graph is a rising slope alveolar plateau if all alveoli had equal amounts of CO2 Phase III would be a flat line 8
Inspiratory Phase 0 Inhalation begins Oxygen fills airway CO2 falls to baseline CO2 is zero Can the ETCO2 Predict Arterial CO2 Levels Alveoli PaCO 2 P ET CO 2 Gradient PaCO 2 P ET CO 2 Gradient Are the PaCO 2, PACO 2, & P ET CO 2 related? PaCO 2 normal = 35 to 45 If all the alveoli in the lung get equal ventilation and perfusion ( V/Q ) PaCO 2 = PACO 2 = P ET CO 2 means there is no alveolar dead space alveolar dead space alveoli without gas exchange alveoli can be ventilated but not perfused alveoli can be perfused but not ventilated similar values for PACO 2 & P ET CO 2 9
PaCO 2 P ET CO 2 Gradient healthy patients a ~ 5 mm Hg difference range of 2 to 5 mm Hg P ET CO 2 < PaCO 2 if PaCO 2 > P ET CO 2 alveolar dead space is present PaCO 2 P ET CO 2 Gradient infants & children g PaCO 2 ~ P ET CO 2 best V/Q ratio & lowest amount of dead space pulmonary embolism alveoli ventilated but not perfused h alveolar dead space PACO 2 is low and now mixes with perfused areas of lung so P ET CO 2 i PaCO 2 P ET CO 2 Gradient h PaCO 2 P ET CO 2 Gradient pulmonary shunts g perfusion but no ventilation collapsed alveoli or fluid in alveoli atelectasis, bronchospasm, edema P ET CO 2 decreases g PaCO 2 P ET CO 2 Gradient h cardiac output h or pulmonary blood flow h PaCO 2 P ET CO 2 Gradient most patients: change in P ET CO 2 correlates to a change in PaCO 2 not as accurate as blood gas or as consistent h in perfusion & P ET CO 2 i in PaCO 2 P ET CO 2 Gradient 10
Normal Values Normal Capnograph Parameter Respiratory Rate Tidal Volume Minute Ventilation P ET CO 2 Adult Range 10-15 breath/min 6 10 ml/kg 4 10 L/min 35 to 45 mm Hg PETCO2 40 mm Hg normal Phase I, II, III normal a and b angles Internet Bing Images Hyperventilation PETCO2 i waveform a low amplitude & narrow respiratory rate h baseline is at zero amplitude is high a high PETCO2 width is wide a slow respiratory rate arterial hypercarbia 11
Apnea Shark Fin Waveform loss of waveform in intubated patient = apnea or dislodged ET non intubated patient complete laryngospasm a immediate onset complete airway obstruction, apnea, mouth breathing Phase III slope has steep rise acute bronchospasm Internet Bing Images Rebreath CO2 Curare Cleft CO2 is not completely washed out causes additional instrument dead space between ET tube and sidestream sampling device malfunctioning exhalation valve exhausted CO2 absorbent CO2 trapped by rubber dam? patient is not completely paralyzed initiates a breath on his own against ventilator most likely due to diaphragm in a spontaneous breathing patient a hiccup, rebreathing, response to pain http://www.capnography.com 12
Cardiac Oscillations Obstruction secondary peaks at end of waveform caused by beating of heart against lungs only seen if respiratory rate is very slow or tidal volume is small indicate inadequate respirations Gravenstein. Capnography 2 nd edition ET tube tube is kinked or obstructed by secretions Spontaneous breathing patient beginning of airway obstruction Anesthesia and Anesthesia & General anesthesia with ET tube capnography verifies correct tube placement crisp waveforms patients with spontaneous respirations get early detection of hypoventilation early intervention prevents significant hypercarbia and respiratory depression 13
Anesthesia & Anesthesia & Open airway techniques SpO2 is excellent for oxygenation SpO2 not adequate for hypoventilation detection your patient can be well oxygenated but be hypercarbic respiratory depression from anesthetic agents requires other monitoring in open airway techniques Opioids & respiratory depression as dose increases a develop slow & irregular respirations at higher doses a decrease in tidal volume result: hypercarbia & hypoxia secondary to alveolar hypoventilation Anesthesia & Intubated patients using capnography detected early and easily corrected increase alveolar ventilations may also need to increase oxygen Open airway techniques stethoscope will detect rate stethoscope can not evaluate tidal volume Anesthesia & Open airway technique without capnography a can develop significant hypercarbia before hypoxia occurs severe hypercarbia will no longer cause central respiratory stimulation get central respiratory depression & possible apnea 14
Respiratory Depression Types of Definition: reduction in alveolar ventilation from a decrease in V T and/ or respiratory rate ( RR ) = arterial hypercarbia Can not diagnose hypoventilation without some measure of alveolar or arterial CO2 Bradypneic hypoventilation decreased minute ventilation ( RR x V T ) iiii RR i V T h ETCO2 Hypopneic hypoventilation decreased minute ventilation ( RR x V T ) iiii V T i RR i ETCO2 Bradypneic Bradypneic respiratory rate is decreased more than V T bradypneic = i respiratory rate i alveolar ventilation h expiratory time h ETCO2 h P A CO2 h PaCO 2 capnograph h amplitude and width normal PaCO 2 P ET CO 2 Gradient bradypneic hypoventilation commonly associated with opioids very slow respiratory rate likely to become hypoxic as it progresses Ann Emerg Med. 2007 15
Bradypneic healthy patients & alveolar hypoventilation no absolute number where hypercapnia will produce apnea PETCO2 > 80 mm Hg are at significant risk of CO2 narcosis & apnea Bradypneic when it first develops SpO 2 shows no desaturation, especially when using supplemental oxygen as alveolar hypoventilation continues will start to see i SpO 2 even with supplemental oxygen need to increase FIO2, cease or reduce drugs, and ventilate the patient Ann Emerg Med. 2007 Hypopneic V T is decreased more than respiratory rate hypopnea = shallow breathing = i depth i alveolar ventilation i ETCO2 ( on capnography unit ) h P A CO2 h PaCO 2 h PaCO 2 P ET CO 2 Gradient Hypopneic waveforms a low amplitude & narrow width low V T does not allow for normal alveolar ventilation and normal exhalation volume so i ETCO2 but h P ACO2 h PaCO 2 16
Hypopneic not uncommon in open airway deep sedation general anesthesia usually due to sedative hypnotics used in anesthesia + opioid if left untreated, you will see i SpO 2 even with supplemental oxygen Annals of Emergency Medicine. 2007; 50(2): 172 Hypopneic hypoventilation Hypopneic variable anesthetic course low tidal volume may resolve as drug redistributes from CNS could cause periodic episodes of apnea could progress to central apnea no respiratory drive SpO 2 will take at least 2 to 3 mins to see a decrease one study: average of 3.7 mins Pediatric Emerg Care. 2011;27(5): 394 hypopneic hypoventilation with pauses treatment reduce dose of agent assess for airway obstruction increase oxygen flow may need to assist ventilations Ann Emergency Med. 2007;50(2):176 17
Bradypneic & Hypopneic Ventilation & Shallow Breathing Type of Bradypneic Hypopneic Resp Rate ( RR ) Tidal Volume ETCO2 iiii i h h i iiii i h PaCO2 normal wave followed by hypopneic hypoventilation i resp rate & i tidal volume stimulate patient to take a deep breath now get alveolar CO2 a h CO2 level Open Airway Deep Sedation Factors leading to hypoxia, apnea, and UAO supine position decreases the FRC by 0.5 to 1.0 liters low V T breathing leads to atelectasis to reduce alveolar ventilation respiratory depression from drugs prevents increases in minute ventilations to correct hypoxia & hypercarbia 18
Anesthesiology 2003; 98: 312 Narcotics and anesthetic agents depress the CNS response to increased levels of Carbon Dioxide Propofol and remifentanil have a profound CNS depressant effect on the CNS response to increased levels of carbon dioxide. When used together, there is a synergistic effect, not additive Anesthesiology 20003; 98: 312 Open Airway Techniques why use capnography? respiratory depression from sedation 17 times more likely to be detected early with capnography than without i in PetCO2 in pediatric sedation with ketamine in ER occurred on average 3.7 minutes before SpO2 changes Anesthesiology 2003; 98:312 J. Clin Anesth. 2011; 23:189 Ped Emerg Care. 2011; 27(5): 394 19
Open Airway Techniques Open Airway Techniques supplemental oxygen masks the detection of hypoventilation by SpO2 should oxygen not be given for moderate sedation to eliminate this deficiency? No, if you don t use oxygen the time between respiratory compromise and desaturation is shortened Pediatrics. 2006; 117(6):e1170 do not expect to see classic waveforms in open airway techniques PetCO2 diluted by O 2 or air patient may be mouth breathing Anesthesiology. 2013;118:192 Nasal Cannula Monitoring Factors that may i accuracy PetCO2 patient secretions & vapor clogging line small tidal volumes tachypnea large volume of sampling line high sampling rates dilution by supplemental oxygen mouth breathing 20
Nasal Cannula Monitoring Dental Anesthesia Problems with dental anesthesia mouth is not closed dilution from mouth breathing supplemental oxygen recommend flow rates of < 3 L/min nasal can not use full face mask nasal airway can be used exceed moderate sedation level do not expect typical intubated waveforms apply cannula prior to sedation to see baseline waveform and numbers diagnosis is based upon changes in baseline not unusual to see no waveform but the patient is breathing Strip #1 21
Strip #5 Strip #6 Strip #7 Identify 22
Strip #8 Strip #9 Strip #10 Interpretation 23
Low amplitude waves? General Anesthesia General Anesthesia Interpretation 24
Interpretation Interpretation Thank you Edward C. Adlesic, DMD Pittsburgh, Pennsylvania eca17@pitt.edu edward_adlesic@msn.com 25