11 capnography


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  • 70% in patients in cardiac arrest– clogged, no CO2-O2 exchange taking place (cellular metabolism) 5%= 35-37 mmHg Yellow could by gastric acid, drugs
  • CO2 enters blood, most diffuses into red blood cells, which contain the enzyme CARBONIC ANHYDRASE. The enzyme catalyzes the reaction of carbon dioxide and water to form carbonic acid: Carbonic acid then dissociates. The Bicarbonate ions diffuse out of the red blood cells into the plasma, leaving HYDROGEN IONS (HEMOGLOBIN BUFFERS THE IONS, CL- (CHLORIDE IONS) enter the red blood cell When the blood reaches the lungs, an area of lower PCO2, these reactions are reversed, CO2 is re-formed and diffuses into the alveoli. Eliminated during exhalation
  • O2 carried by weak bond with hemoglobin (98.5%) each hemoglobin can bind FOUR molecules of O2 (HbO2) oxyhemoglobin 10%= dissolved in blood 20%= HbCO2= carbaminohemoglobin 70%= bicarbonate ions
  • Stroke volume- amount of blood ejected by the left ventricle with each contraction approximately 60-80ml. Varies with age, sex, health. Tidal volume- amount of air inspired and expired in a normal breath.
  • Low cardiac output caused by cardiogenic or hypovolemia resulting from hemorrhage wont carry as much co2 back to the lungs, resulting in lower co2. Doesn’t mean the pt is hyperventilating, or their arterial co2 level will be reduced. Reduced perfusion to the lungs alone causes this phenomenon. Lung function is perfectly normal.
  • Beta angle increases with rebreathing
  • Hydrogen cyanide byproduct of combustion, plastics in house fires. CO= Leading cause of death from fire. Hemoglobin’s affinity for CO is over 240 times greater than O2. CO forms CARBOXYHEMOGLOBIN (COHb)
  • Stop compressions for 20 seconds decreased survival by 50%.
  • A sudden rise in EtCO 2 indicates increased cardiac output. Cardiac output immediately after ROSC is often low and drugs such as epinephrine can produce peripheral vasoconstriction, so palpating a pulse may be very difficult. The presence of an organized rhythm on the monitor accompanied by a sudden increase in EtCO 2 indicates ROSC has occurred and cardiac output has improved despite questionable pulses.
  • Hypercapnia causes cerebral vasodilation, which causes increased CBF, and further elevates ICP. Hypocapnia causes cerebral vasoconstriction, reduce ICP. Resulting in hypoperfusion. MAP-ICP=CPP
  • 11 capnography

    1. 1. CAPNOGRAPHY presented by: Fred Halazon , NREMT-P Mike Burke , NREMT-P Cunningham Fire
    2. 2. What is Capnography? <ul><li>Noninvasive, continuous measurement of exhaled carbon dioxide concentration over time </li></ul><ul><li>Digital display provides EtCO 2 value </li></ul><ul><li>Provides a distinct waveform for each respiratory cycle </li></ul>
    3. 4. Overview <ul><li>History </li></ul><ul><li>Anatomy & Physiology </li></ul><ul><li>Capnographic waveform </li></ul><ul><li>Diagnosing different waveforms </li></ul><ul><li>Case studies </li></ul>
    4. 5. Relevance <ul><li>ETT Verification </li></ul><ul><li>Cardiac Arrest </li></ul><ul><li>Ventilation </li></ul><ul><li>Bronchospastic Disease </li></ul><ul><li>Early detection of cellular hypoxia </li></ul>
    5. 6. History of capnography <ul><li>Used by anesthesiologists since the 1970s </li></ul><ul><li>Standard of care in the OR since 1991 </li></ul>
    6. 7. History of Capnography in EMS <ul><li>Colormetric- Useful device to confirm ET tube placement in patients not in cardiac arrest </li></ul><ul><li>Tube could be in esophagus or that circulation is not bringing CO 2 to the lungs </li></ul><ul><li>Prone to contamination, leads to false negatives </li></ul>
    7. 8. History of Capnography in EMS <ul><li>Pulse oximetry preceded capnography </li></ul><ul><li>Pulse oximetry measures oxygenation </li></ul><ul><li>Capnography measures ventilation </li></ul><ul><li>New technologies now allow use in EMS </li></ul>
    8. 9. Capnometry <ul><li>Provides only a numerical measurement of carbon dioxide ( EtCO 2 ) </li></ul>
    9. 10. Capnogram <ul><li>A waveform display of carbon dioxide over time </li></ul>
    10. 11. Definition of Capnography <ul><li>Numerical value of the EtCO 2 AND </li></ul><ul><li>Waveform of the concentration present in the airway </li></ul><ul><li>Respiratory rate detected from the actual airflow </li></ul>
    11. 12. Definitions <ul><li>PACO 2 —Partial pressure of CO 2 in the alveoli </li></ul><ul><li>PaCO 2 —Partial pressure of CO 2 in arterial blood </li></ul><ul><li>PEtCO 2 —Partial pressure at the end of expiration </li></ul><ul><li>PvCO 2 —Partial pressure of CO 2 in mixed venous blood </li></ul><ul><li>PCO 2 —Partial pressure of CO 2 </li></ul>
    12. 13. Definitions <ul><li>PaO 2 —Partial pressure of O 2 in arterial blood (hypoxemia) </li></ul><ul><li>SPO 2 —Saturation of arterial blood (POX) percent </li></ul><ul><li>SaO 2 —Percentage of arterial hemoglobin saturated with O 2 (POX) </li></ul><ul><li>PO 2 —Partial pressure of O 2 </li></ul>
    13. 14. What is Carbon Dioxide? <ul><li>Capnos comes from the Greek word for “smoke” </li></ul><ul><ul><li>Smoke from the Fire of metabolism </li></ul></ul><ul><ul><li>Natural waste product of cellular activity </li></ul></ul><ul><li>CO 2 is a compound molecule </li></ul><ul><ul><li>2 elements of oxygen and 1 element of carbon </li></ul></ul><ul><ul><li>Colorless and heavier than air </li></ul></ul>
    14. 15. Carbon Dioxide Transport <ul><li>CO 2 + H 2 O H 2 CO 3 </li></ul><ul><li>Carbonic acid dissociates: </li></ul><ul><li>H 2 CO 3 H + + HCO 3 _ </li></ul>
    15. 16. Gas Transport in Blood <ul><li>O 2 carried in blood </li></ul><ul><ul><li>Dissolved in blood plasma </li></ul></ul><ul><ul><li>Bound to hemoglobin with iron </li></ul></ul><ul><li>CO 2 carried in blood </li></ul><ul><ul><li>Dissolved in plasma (5-10%) </li></ul></ul><ul><ul><li>Chemically bound to hemoglobin in (RBC’s) (carbaminohemoglobin) (20-30%) </li></ul></ul><ul><ul><li>Most carried as bicarbonate ions (HCO3-) (60-70%) </li></ul></ul>
    16. 17. Physiology of CO 2 <ul><li>End of inspiratory cycle, airways filled with CO 2 free gas </li></ul><ul><li>CO 2 is a product of cellular metabolism </li></ul><ul><li>CO 2 is continuously diffused across the cell membrane into the circulating blood </li></ul>
    17. 18. Physiology of CO 2 <ul><li>Transported to the lungs in the blood stream </li></ul><ul><li>Diffused across cell membrane into alveoli </li></ul><ul><li>Eliminated during exhalation </li></ul>
    18. 19. Oxygen > lungs> alveoli> blood Muscles + organs Oxygen + Glucose O 2 CO 2 CO 2 CO 2 O 2 cells energy blood lungs breath
    19. 21. Physiology of CO 2 <ul><li>The evolution of CO 2 from the alveoli to the mouth during exhalation, and inhalation of CO 2 free gases during inspiration gives the characteristic shape to the CO 2 curve which is identical in all humans with healthy lungs </li></ul>
    20. 22. Capnographic Waveform Expiration Inspiration Inspiration
    21. 23. Physiology of CO 2 <ul><li>Alveoli in lower lung is more perfused, but less ventilated </li></ul><ul><li>In the more proximal respiratory tract, the CO 2 falls gradually to zero at some point </li></ul>
    22. 24. 0 36 40 44
    23. 25. Physiology of CO 2 <ul><li>Concentration of CO 2 in alveoli is determined by: </li></ul>PERFUSION (Q) VENTILATION (V)
    24. 26. Physiology of CO 2 <ul><li>Concentration of CO 2 in alveoli: </li></ul><ul><li>Varies INDIRECTLY with ventilation </li></ul><ul><li>Increase Ventilation: Decrease CO 2 in Alveoli </li></ul><ul><li>Decrease Ventilation: Increase CO 2 in Alveoli </li></ul><ul><li>Varies DIRECTLY with perfusion </li></ul><ul><li>Decrease Perfusion: Decrease CO 2 in Alveoli </li></ul><ul><li>Increase Perfusion: Increase CO 2 in Alveoli </li></ul>
    25. 27. Oxygenation and Ventilation What is the difference? <ul><li>Oxygenation : is the transport of O 2 via the bloodstream to the cells </li></ul><ul><ul><li>Oxygen is required for metabolism </li></ul></ul><ul><li>Ventilation : is the movement of air into and out of the lungs </li></ul><ul><ul><li>exhaling of CO 2 via the respiratory tract </li></ul></ul><ul><ul><li>Carbon dioxide is a byproduct of metabolism </li></ul></ul>
    26. 28. Oxygenation <ul><li>Measured by pulse oximetry (SpO 2 ) </li></ul><ul><ul><li>Noninvasive measurement </li></ul></ul><ul><ul><li>Percentage of oxygen in red blood cells </li></ul></ul><ul><ul><li>Changes in ventilation take several minutes to be detected </li></ul></ul><ul><ul><li>Affected by motion artifact, poor perfusion, temperature </li></ul></ul>
    27. 29. Ventilation <ul><li>Measured by the end-tidal CO 2 </li></ul><ul><ul><li>Partial pressure (mm Hg) or volume (%) of CO 2 in the airway at end of exhalation </li></ul></ul><ul><ul><li>Breath-to-breath measurement provides information within seconds </li></ul></ul><ul><ul><li>Not affected by motion artifact, distal circulation, temperature </li></ul></ul>
    28. 30. Distinguishing between oxygenation and ventilation
    29. 31. Normal Ventilation/Perfusion Ratio <ul><li>The volume of blood returning to the lungs matches the capacity of the lungs to exchange gases </li></ul><ul><li>Ventilation </li></ul><ul><li>Cardiac Output </li></ul>
    30. 32. Ventilation-Perfusion (V/Q) Mismatch <ul><li>Phenomenon where either perfusion or ventilation to an area of lung decreases; results in diminished gas exchange, hypoxemia, and hypercapnia </li></ul>
    31. 33. <ul><li>If ventilation is held constant, then changes in EtCO 2 are due to changes in cardiac output </li></ul>
    32. 34. 36 5 32 4 28 3 20 2 EtCO2 (mm Hg) Cardiac Output (L)
    33. 36. Break
    34. 37. Value of the Capnographic Waveform <ul><li>Provides valid EtCO 2 value </li></ul><ul><li>Visual assessment of patient airway integrity </li></ul><ul><li>Verify proper ET tube placement (with pulmonary perfusion) </li></ul><ul><li>Waveforms have characteristic shape like an ECG </li></ul>
    35. 38. Capnographic Waveform <ul><li>Height shows amount of CO 2 </li></ul><ul><li>Length depicts time </li></ul>
    36. 39. Phases of Capnogram Expiratory segment <ul><li>Consists of the following three phases </li></ul>
    37. 40. Phase I <ul><li>Phase I - Represents CO 2 free gas from airways (Dead Space) </li></ul>
    38. 41. Phase I Beginning of exhalation A B I
    39. 42. Phase II <ul><li>Phase II - Consists of rapid upswing (due to mixing of dead space gas with alveolar gas (Ascending Phase) </li></ul>
    40. 43. Phase II II A B C Ascending Phase
    41. 44. Phase III <ul><li>Phase III - Consists of an alveolar plateau, CO 2 rich gas, positive slope, rise in PCO 2 (Alveolar Plateau) </li></ul>
    42. 45. Phase III A B C D I I I Alveolar Plateau
    43. 46. Slope of Phase III <ul><li>CO 2 is being continuously excreted into the alveoli </li></ul><ul><li>Late emptying of alveoli with lower (V/Q) ratios, produces higher PCO 2 </li></ul><ul><li>End-tidal </li></ul><ul><ul><li>End of the wave of exhalation </li></ul></ul>
    44. 47. Expiratory segment cont… <ul><li>Alpha angle - Angle between phase II and phase III (V/Q status of lung) </li></ul>
    45. 48. Phases of Capnogram Inspiratory segment <ul><li>Beta Angle - Angle between phase III and descending limb of inspiratory segment </li></ul>
    46. 49. Inspiratory segment <ul><li>Phase 0 - Inspiration, fresh gases inhaled and CO 2 falls rapidly to zero (Descending Phase) </li></ul>
    47. 50. Phase 0 A B C D E 0 Descending Phase Inhalation
    48. 51. End-tidal CO 2 (EtCO 2 ) <ul><li>Allows monitoring for changes in </li></ul><ul><ul><li>Ventilation —Asthma, COPD, airway edema, FBAO, stroke </li></ul></ul><ul><ul><li>Diffusion —Pulmonary edema, alveolar damage, CO poisoning (COHb), smoke inhalation, hydrogen cyanide </li></ul></ul><ul><ul><li>Perfusion —shock, pulmonary embolus, cardiac arrest, severe dysrhythmias </li></ul></ul>
    49. 52. Decreased EtCO 2 <ul><li>Decreased Metabolism </li></ul><ul><ul><li>Analgesia/ sedation </li></ul></ul><ul><ul><li>Hypothermia </li></ul></ul><ul><li>Circulatory System </li></ul><ul><ul><li>Cardiac arrest </li></ul></ul><ul><ul><li>Embolism </li></ul></ul><ul><ul><li>Sudden hypovolemia or hypotension </li></ul></ul><ul><li>Respiratory System </li></ul><ul><ul><li>Alveolar hyperventilation </li></ul></ul><ul><ul><li>Bronchospasm </li></ul></ul><ul><ul><li>Mucus plugging </li></ul></ul><ul><li>Equipment </li></ul><ul><ul><li>Leak in system </li></ul></ul><ul><ul><li>Partial obstruction </li></ul></ul><ul><ul><li>ETT in hypopharynx </li></ul></ul>
    50. 53. Increased EtCO 2 <ul><li>Increased Metabolism </li></ul><ul><ul><li>Pain </li></ul></ul><ul><ul><li>Hyperthermia </li></ul></ul><ul><ul><li>Malignant hyperthermia </li></ul></ul><ul><ul><li>Shivering </li></ul></ul><ul><li>Circulatory System </li></ul><ul><ul><li>Increased cardiac output with constant ventilation </li></ul></ul><ul><li>Respiratory System </li></ul><ul><ul><li>Respiratory insufficiency </li></ul></ul><ul><ul><li>Respiratory depression </li></ul></ul><ul><ul><li>Obstructive lung disease </li></ul></ul><ul><li>Equipment </li></ul><ul><ul><li>Defective exhalation valve </li></ul></ul><ul><ul><li>Exhausted CO 2 absorber </li></ul></ul>
    51. 54. Major Benefits in Pre-Hospital <ul><li>Verifying ETT placement and continuous monitoring of position during transport </li></ul><ul><li>Cardiac Arrest </li></ul><ul><ul><li>Effectiveness of cardiac compression </li></ul></ul><ul><ul><li>Predictor of survival </li></ul></ul><ul><li>Ventilation </li></ul><ul><li>Bronchospastic Disease </li></ul>
    52. 55. Benefits in Hospital <ul><li>Verification of ETT placement and continuous monitoring </li></ul><ul><li>Cardiac Arrest </li></ul><ul><li>Ventilation </li></ul><ul><li>Procedural sedation </li></ul>
    53. 56. ETT Displacement Most likely occurs when patient is moved
    54. 57. Dislodged
    55. 58. Dislodged
    56. 59. Right Main Bronchi
    57. 60. CPR <ul><li>Force, depth, and rate of chest compressions </li></ul>100% mortality if unable to achieve an EtCO2 of 10 mm Hg after 20 minutes 4 5 0
    58. 61. CPR
    59. 62. ROSC
    60. 63. ROSC 4 5 0
    61. 64. ROSC with NaHCO 3
    62. 65. CPR <ul><li>Positive pressure ventilation </li></ul><ul><li>Increased intrathoracic pressure </li></ul><ul><li>Pressure on Vena Cava, decreased preload </li></ul><ul><li>Increased RR does not allow for exhalation </li></ul>
    63. 66. CPR <ul><li>Increased intrathoracic pressure leads to </li></ul><ul><li>Decrease in cardiac output, coronary artery perfusion, and CPP </li></ul>
    64. 68. Optimize Ventilation <ul><li>Titrate carbon dioxide levels in patients sensitive to fluctuations </li></ul><ul><ul><li>Head Injuries </li></ul></ul><ul><ul><li>Stroke </li></ul></ul><ul><ul><li>Brain tumors </li></ul></ul><ul><ul><li>Brain infections </li></ul></ul>
    65. 69. Optimize Ventilation <ul><li>Carbon dioxide affects cerebral blood flow (CBF) </li></ul><ul><ul><li>Influencing intracranial pressure </li></ul></ul><ul><ul><li>Hypercapnia causes vasodilation </li></ul></ul><ul><li>Hyperoxygenate, NOT hyperventilate </li></ul><ul><ul><li>Hyperventilation does not improve oxygenation </li></ul></ul><ul><ul><li>Maintain CO 2 of 35-40 mm Hg </li></ul></ul>
    66. 71. Hyperventilation <ul><li>Hypocapnia < 35 mmHg </li></ul><ul><li>Normal range is 35-45 mm Hg (5% vol) </li></ul><ul><li>How would hyperventilation change the waveform? (26-30) </li></ul><ul><ul><li>Frequency </li></ul></ul><ul><ul><li>Duration </li></ul></ul><ul><ul><li>Height </li></ul></ul><ul><ul><li>Shape </li></ul></ul>
    67. 72. Hyperventilation 4 5 0
    68. 73. Hypoventilation <ul><li>Hypercapnia > 45 mmHg </li></ul><ul><li>How would hypoventilation change the waveform? (4-12) </li></ul><ul><ul><li>Frequency </li></ul></ul><ul><ul><li>Duration </li></ul></ul><ul><ul><li>Height </li></ul></ul><ul><ul><li>Shape </li></ul></ul>
    69. 74. Hypoventilation 4 5 0
    70. 75. Bronchospasm <ul><li>Alveoli unevenly ventilated on inspiration </li></ul><ul><li>Asynchronous emptying during expiration </li></ul><ul><li>Alters Phase II— </li></ul><ul><ul><li>“Shark Fin” shaped waveform </li></ul></ul>
    71. 76. Bronchospasm 4 5 0 Bronchospasm
    72. 77. Bronchospasm
    73. 78. COPD
    74. 79. Asthma Initial After therapy
    75. 80. Pneumothorax
    76. 81. Pulmonary Embolism
    77. 82. Hypercapnia/ RR~?
    78. 83. 15 Sec Triage Tool <ul><li>Rapidly assess pt </li></ul><ul><li>Toxins, chemical agents </li></ul><ul><li>Spontaneous respirations </li></ul><ul><li>Patent airway with adequate ventilation and perfusion </li></ul><ul><li>Most acute pts </li></ul><ul><li>Seizures </li></ul>
    79. 84. 15 Sec Triage Tool <ul><li>Terrorism (BNICE) </li></ul><ul><li>Absorption skin and respiratory tract </li></ul><ul><li>Respiratory depression </li></ul><ul><li>Trends </li></ul>
    80. 87. Unresponsive patients
    81. 88. 6 year old female <ul><li>Status seizure </li></ul><ul><li>Found supine in bed with L disconjugate gaze </li></ul><ul><li>Unresponsive to stimuli </li></ul><ul><li>Vomiting </li></ul><ul><li>B/P- 136/66 </li></ul><ul><li>HR- 136 </li></ul><ul><li>RR- 40 </li></ul><ul><li>Skin- warm, dry, acyanotic </li></ul>
    82. 89. 6 year old <ul><li>Tx pt to pram controlling airway </li></ul><ul><li>Supplemental O2 </li></ul><ul><li>Unable to establish IV </li></ul><ul><li>Administer 5mg Valium PR </li></ul><ul><li>B/P- 108/70 </li></ul><ul><li>HR- 116 </li></ul><ul><li>RR- 36 </li></ul>
    83. 90. 6 year old <ul><li>Heent- Clr </li></ul><ul><li>Perrla </li></ul><ul><li>Chest = rise/fall w/clr BS B/L </li></ul><ul><li>ABD= snt </li></ul><ul><li>Pelvis= stable </li></ul><ul><li>SmoeX4 w/o angulation </li></ul><ul><li>Back Clr </li></ul><ul><li>No visual signs of Trauma </li></ul>
    84. 91. 6 year old <ul><li>No recent medical hx or illnesses </li></ul><ul><li>NKDA </li></ul><ul><li>Clonidine for sleep aid at night </li></ul><ul><li>Capnographic waveform </li></ul>
    85. 92. EtCO2: 50 RR: 36
    86. 93. Decreased Cardiac Output <ul><li>94 y.o. Female </li></ul><ul><li>DNR </li></ul><ul><li>Respiratory distress </li></ul><ul><li>Skin- ashen, cool, dry </li></ul>
    87. 94. HR: 31 EtCO2: 8 RR: 7
    88. 95. Case <ul><li>35 y.o. male </li></ul><ul><li>DK, combative </li></ul><ul><li>Possible OD </li></ul>
    89. 96. EtCO2: 34 RR: 33
    90. 98. Documentation <ul><li>Continuous waveform allows for legal documentation </li></ul><ul><li>Proof of correct tube placement, RR, EtCO 2 </li></ul><ul><li>Effectiveness of treatment in patient care, early detection of deterioration </li></ul>
    91. 99. <ul><li>The era is over when we can justify not knowing whether an ETT is in place or not. </li></ul><ul><li>We may not be able to intubate everybody, but we must always know when the tube is in place or not. </li></ul>
    92. 100. Break Time
    93. 101. What is up coming and how Capnography will assist <ul><li>The newest phase in CPR Protocols. </li></ul><ul><li>How it will effect our decisions to work a patient or not. </li></ul><ul><li>The CPR first protocols. </li></ul><ul><li>Therapeutic Hypothermia. </li></ul>
    94. 102. What is Therapeutic Hypothermia <ul><li>Is an evidence based change in Cardiac Arrest patients </li></ul><ul><li>This change effects treatment of the patient with a return to spontaneous pulses. </li></ul><ul><li>The studies show good stats that back up this method of treating patients </li></ul>
    95. 103. The European Study <ul><li>This study was conducted in Nine hospitals and 5 countries. </li></ul><ul><li>The Study was performed completely random. </li></ul><ul><li>The patients were accepted into the study based on speed of response to V-fib arrest. </li></ul>
    96. 104. The Australian study <ul><li>Less involved study. </li></ul><ul><li>This study took place in Melbourne and involved four hospitals </li></ul><ul><li>This study was done Pseudo random format with patients selected based on an odd or even day. </li></ul>
    97. 105. Criteria <ul><li>The patient to be accepted into the study had to be a persistent V-fib arrest and still in coma state u/a to hospital. </li></ul><ul><li>The patient must have Resuscitation efforts performed by trained personnel within 5-15 minutes of collapse. </li></ul><ul><li>The patient must also have ROSC in under sixty minutes. </li></ul><ul><li>The patient must also be intubated and ventilated. </li></ul>
    98. 106. European Study Procedures <ul><li>The patient was cooled to 32 to 34 degrees Celsius. </li></ul><ul><li>This temp was reached in the first four hours of the resuscitation. </li></ul><ul><li>Pt was held at this temp for twenty four hours and then passively re-warmed. </li></ul>
    99. 107. Australian Study <ul><li>Pt. Accepted on the same criteria however it was based on if it was an odd or even day. </li></ul><ul><li>The pt were cooled to 33 degrees Celsius and kept there for 12 hours and the actively re-warmed after 18 hours. </li></ul>
    100. 108. The Results and they were impressive! <ul><li>In the European Study 75 of 136 patients(55%) had a favorable neurological outcome. </li></ul><ul><li>In the normothermic patients the results were still good but not great at 39% </li></ul><ul><li>The Australian Study showed a 49% save rate in the hypothermic pt and a 26% in the normothermic pt. </li></ul>
    101. 109. Why do this work? <ul><li>The proof is in the pudding for its benefits. </li></ul><ul><li>However the actions is slightly more theoretical. </li></ul><ul><ul><li>Fist is hypothermia lowers the cerebral metabolic rate for oxygen by 6% for every 1 degree C </li></ul></ul><ul><ul><li>Second hypothermia suppresses chemical reactions. </li></ul></ul>
    102. 110. If this so great why don’t we use it! <ul><li>Simple Logistics </li></ul><ul><li>The patient once taken to the hypothermic state must remain there to have benefit. A Rolla coaster approach is not going to work. </li></ul><ul><li>The equipment to do this efficiently and controlled is expensive but is expected to fall in price as it becomes more widely spread. </li></ul>
    103. 111. <ul><li>Barton, C. & Wang, E. (1994). Correlation of End-Tidal CO2 Measurements to Arterial PaCO2 in Nonintubated Patients. Annals of Emergency Medicine, 23 (3): 561-562. </li></ul><ul><li>Bergenholtz, K.F., RN, MSN, CRNP-CS. (2004). Using and understanding Capnography. Microstream capnography solutions. [email_address] </li></ul><ul><li>Bhavani-Shankar, K., MD, Philip, JH. Defining segments and phases of a time capnogram. Anesthesiology Analg (2000). 91(4): 973-977. </li></ul><ul><li>Bhavani-Shankar, K., MD. http://capnography.com/ </li></ul><ul><li>Falk, J.L., Rackow, E.C., Weil, M.H. End-tidal carbon dioxide concentration during cardiopulmonary resuscitation. New England Journal of Medicine (1998) 318(10): 607-611. </li></ul><ul><li>Fowler, Ray, MD, FACEP. www.rayfowler.com </li></ul><ul><li>Fowler, W.S. Lung Function studies, II. The respiratory deadspace. American Journal of Physiology. (1998) 154: 405-416. </li></ul><ul><li>Kanowitz, A., MD, FACEP, EMS Director, Arvada, CO. (2004). [Capnography in EMS]. Unpublished raw data. </li></ul>References
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