Carbon Dioxide Physiology


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Carbon Dioxide Physiology

  1. 1. Carbon Dioxide Physiology & Hypoxemia Nick Ford, DO
  2. 2. Carbon DioxideTwo dissimilar atoms, one carbon atom with twodoubly bonded oxygen atomsProduct of cellular metabolism in mammalsCan diffuse readily across cellular membranes 20 times as easy as oxygen
  3. 3. TransportModes of transportation in the blood Bicarbonate (HCO3-) Carbamino-hemoglobin Dissolved CO2 In physical solution
  4. 4. DetectionCapnography Utilizes infrared radiation to detect the carbon and oxygen atomsCan detect esophageal intubation, Not detect endobronchial intubation
  5. 5. Universal Capnography. A vital asset that can improve patient care on almost any call. Elements of a Waveform Patricia A. Brandt, RN, BSN, MHR2009 Mar 1A-B: respiratory baseline, begin exhalation, dead space removing CO2-free gasB-C: continued exhalation,  CO2 rich + mix dead spaceC-D: represents an approach to end-exhalation “alveolar plateau” with nearlyconstant rich CO2 gasD: point at which during exhalation that CO2 is at the highest concentrationD-E: inspiration
  6. 6. Capnogram Variations Sudden decrease to zero: Considered equipment problem, possible disconnect Sudden decrease but not to zero: Consider a leak or an obstruction (partial) of airway or system Exponential decrease: Increased dead space; possible causes are PE, cardiac arrest Sudden increase: Consider tourniquet release Gradual increase: Consider decreased minute ventilation, prolapsed expiratory valve
  7. 7. Ventilatory Control Central Response Peripheral ResponseMedulla Hypoxemia Triggers Response CN IX (glossopharyngeal) Afferent limb (PaO2 < 60mmHg) CN X (vagus) Efferent limb Carotid bodies Respond via ventilationIncreased PaCO2 tension Causes CO2 passes through blood-brain-barrier Aortic bodies Acid (H+) is then formed Respond via circulatory creating acidosis d/t lack of buffering changes MV increased w/ depth, rate increasesPaCO2 > 100mmHg will become arespiratory depressant
  8. 8. ApneaNormal PaCO2 is 36-44mmHg (sea level)Apnea Results in a 6mmHg increase CO2 during the first minute and 3mmHg increase CO2 for each subsequent minute thereafterETCO2 correlation to PaCO2 Difference of 5mmHg in normal patient, difference increases with increased dead spaceApneic Threshold a point in which a maximum PaCO2 level is achieved without initiating spontaneous ventilation Approximately 5mmHg below resting PaCO2
  9. 9. CO2 Response CurvePlots MV in L/min along the Y-axis and PaCO2 mmHgalong the X-axisRightward shift  or a downward andrightward shift  implies suppression ofventilationLeftward  and leftward and upward implies stimulation of ventilation
  10. 10. Effects on the CO2 Response Curve Leftward Rightward  Occur d/t  sensitivity to CO2 Occur d/t  sensitivity to CO2secondary to causes: secondary to causes: Metabolic alkalemia Metabolic acidemia Normal sleep Central (anxiety, fear,  ICP, cirrhosis) Hypothermia Denervated peripheral Arterial hypoxemia receptors Rx Drugs Doxapram, analeptics, stry Catecholamines, salicylates chnine , aminophylline
  11. 11. Effects on the CO2 Response CurveDownward and to the Right Sedatives, barbiturates, volatile anesthetics, opiates
  12. 12. CO2 Response Curve Control of Breathing
  13. 13. Hypercarbia - arterial carbon dioxide tension > 45mmHg Hypoventilation  CO2 Production compliance O2 consumption goes hand-in- hand with CO2 production respiratory drive (2nd tocentral anesthetic effect) Hyperthermia (≥40°C) and MHSurgical positioning Hyperthyroid Hyperalimentation Shivering Catecholamine release
  14. 14. Hypercarbia continued…  Dead Space Ventilation Inspired CO2(Not participant of gas exchange) Direct CO2 in circuit PEEP may increase Zone 1 Exhausted CO2 absorber ventilation Rebreathing CO2 if fresh gas Anesthesia circuit system flow is low 33-46%  intubated patient 64%  when ventilated by mask Laparoscopic procedures with PE, thrombosis CO2 insufflation Rapid, shallow respirations
  15. 15. Complications of Hypoventilation-hypercarbiaRightward shift  oxy-hemoglobin dissociation curve PA pressure (CO2 is pulmonary Vc; most other locations a Vd) Cerebral blood flow  or  1ml/100g/min for every mmHg  or  PaCO2 from baselineAcidosisArrhythmiasEpi-norepi release resulting in Splanchnic Vc, cutaneous VdSympathoadrenal system stimulation in respond tocardiac/vascular depressionPreterm infants will have smaller increases in MVIncreased uterine blood flow at PaCO2 >60mmHg
  16. 16. Complications of Hyperventilation-hypocarbiaLeftward  shift oxy-hemoglobin dissociation curveV/Q mismatchApnea CBF, CO, Ca,  coronary BF
  17. 17. OxygenOxygen exists as dissolved in the blood or as boundto hemoglobinO2 Content = (1.34 x Hb) * SaO2 SaO2: percentage volume of oxygen attached to hemoglobin [CaCO2=(1.34 * HgB * Sat) + (0.003 *PaO2)]Final electron acceptor in electron transport chain inmitochondria, permitting life/metabolism
  18. 18. Oxygen DetectionSaturation Frequently measured by pulse oximetry False elevations Carboxyhemoglobin and methemoglobin (until 85%) have similar absorption spectrum as oxyhemoglobin; can be difficult to detect difference Fluoroescent lighting False depression Tape Blue nail polish Dyes- indigo carmine, methylene bluePartial pressure ABG
  19. 19. HypoxemiaDefined simply as decreased arterial oxygen tensionin the blood below 60mmHg
  20. 20. curve*Clinical Arterial Blood Gas Analysis. Written Board P.R.E.P. BigBlue. 2003. Neils Jensen . Oxygen dissociation
  21. 21. Oxygendissociation P50 Parital pressure of O2 where Hgb is 50% saturated adults = 27mmHg Infants = 19mmHg A : nml mixed venous B : 90% saturation = 60mmHg
  22. 22. Oxygen Dissociation Curve Left Shift  Right Shift  release of O2 from Hgb  release of O2 from Hgb Alkalosis Acidosis  temperature  temperature 2,3-BPG 2,3-BPG (states d/t methemoglobin anemia, altitude, cirrhosis)  CO2Haldane effect: Bohr effect: Deoxygenated blood (reduced Hgb) carries more CO2 in O2-Hgb curve shifts d/t Δ’s in carbamino compounds – no Δ in CO2 PaCO2
  23. 23. Mixed Venous O2 levelsSampling from Pulmonary arteryProvides insight to tissue oxygen deliveryNormal PvO2 = 35-45mmHg with SaO2 65-75%Factors that influence PvO2 Loading/unloading of O2 by Hgb O2 utilization Hgb present Cardiac output
  24. 24. Causes of HypoxemiaDecreased FiO2HypoventilationV/Q mismatch / ShuntAbsolute shunt (V/Q=0)Diffusion abnormalityAnemia / PoisoningHypovolemiaIntrapulmonary derangements
  25. 25. Decreased FiO2Level adjusted too lowPossible mechanical or technical failure of anesthesiamachine or ventilatory apparatusN2O washout N2O is 35x more soluble than nitrogen The washout occurs as N2O leaves the bloodstream faster than O2 can enter, thereby dilluting the PAO2 and creating hypoxia
  26. 26. HypoventilationRespiratory Depression Drugs Paralysis COPD may decrease their hypercapneic ventilatory drive Carotid bodies- may become desensitized in carotid artery diseaseHabitusThoracic / Upper abdominal incisionsAirway obstruction Airway class Sedation vs GA w/ airway deviceEquipment Blocked tube Disconnect Ventilator malfunction
  27. 27. V/Q Mismatch & Shunt FRC- GA reduces by about Increased airway resistance400ml in adult Bronchospasm Supine- decreases by another 800ml One-lung ventilation Obesity, pregnancy, abdominal sx, ascites Surgical clamping or Large  FRC may cause end- compression expiratory volumes below closing capacity Pneumonia also  pulmonary compliance closing capacity (equal toclosing volume + residual volume)  w/ smoking, obesity, LVF, Age, Surge ry, Chronic bronchitis
  28. 28. Absolute ShuntPerfused without ventilationDoes not improve with  O2 deliveryNormal physiologic shunt is about 2-5% of overall CO
  29. 29. Diffusion abnormalityrare
  30. 30. HypoxemiaAnemia / Poisoning Low Cardiac OutputMethemoglobinemia Hypovolemia Blood lossCarbon Monoxide Most efficient way to improve oxygenation is toNitroprusside toxicity  hemoglobin Cytochrome oxidase binds CN-, thus inhibiting aerobic High SVR metabolism Cardiogenic Shock
  31. 31. Intrapulmonary DerangementsBronchospasmEmbolism PE Fat embolus Gas embolusPulmonary edemaPneumothoraxAspirationAtelectasis
  32. 32. Hypoxic Pulmonary VasoconstrictionPulmonary Vc in response to regional lung hypoxiaMinimizes shunt,  flow up to 50%
  33. 33. Advice to Those Taking the Re-certification Exam Review Material and Question Books Carbon Dioxide; Clinical Arterial Blood Gas Analysis; Hypoxemia; Respiratory. Written Board P.R.E.P. Big Blue. 2003. Neils Jensen. Review of Clinical Anesthesia. Connelly & Silverman. Lippincott Williams & Wilkins. Appleton & Lange Board Review of Anesthesiology. Mark Dershwitz. McGraw Hill.
  34. 34. ReferencesUniversal Capnography. A vital asset that can improvepatient care on almost any call. PatriciaA. Brandt, RN, BSN, MHR2009 Mar 1.Control of Breathing Dioxide; Clinical Arterial Blood Gas Analysis;Hypoxemia; Respiratory. Written Board P.R.E.P. Big Blue.2003. Neils Jensen.Anesthesia Secrets 2nd Edition, 2000. James Duke, MD.Haley & Belfus, Inc.