Ventura la ttt
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The document outlines the Advanced Resuscitation Techniques (ART) model for improving resuscitation outcomes. It describes seven commandments of cardiac arrest care, including high-quality chest compressions, use of pressors, ventilation techniques, and a focus on prevention. Sample patient cases and data on outcomes with the ART model in San Diego show increased survival rates from cardiac arrest.
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Ventura la ttt
- 1. Daniel Davis, MD UCSD Center for Resuscitation Science ART: A New Model of Resuscitation
- 4. UCSD Center for Resuscitation Science People should not die before they are done living.
- 6. Elevated life support training from a regulatory requirement into the primary vehicle for addressing all resuscitation-related issues.
- 10. Integrated Critical Care Model PART BART ART HeART TART RAT AART PhART
- 11. Arrest Survival
- 12. Arrest Survival
- 13. Prevention
- 15. Arrest Incidence
- 16. Arrest Survival
- 17. Overall Impact
- 19. ART responsible for more than 85% of the decrease! Overall Impact
- 21. CPR in Progress
- 22. San Diego EMS Baseline Training #1 Training #2
- 23. El Cajon Cardiac Arrests 1.6% Survival 9.0% Survival Cogntiive training
- 26. Airway Management Preoxygenation Approach
- 28. Traumatic Brain Injury 83.3% 80.6% 78.5%
- 29. Cardiac Arrest
- 32. Prime the Pump! Kern (2002) Circulation
- 33. Stay on the chest! Christenson (2009) Circulation * Adjusted for: age, gender, bystander CPR, public location, response time, compression rate
- 35. Bystander CPR
- 36. Stiell et al (2008) AHA Scientific Sessions Deeper Compressions
- 37. Aufderheide (2005) Resuscitation Recoil?
- 38. CPR Process Data
- 41. Return of Spontaneous Circulation Electrical (HR) Mechanical (PetCO2)
- 42. Lung Perfusion in Shock
- 43. PaCO2 40 mmHg PetCO2 37 mmHg 40 40 40 40 40 40
- 44. PaCO2 40 mmHg PetCO2 23 mmHg 0 40 40 40 0 40
- 45. PaCO2 40 mmHg PetCO2 11 mmHg 0 40 0 40 0 0
- 46. Capnometry
- 48. Case
- 53. ROSC Predictors HR EtCO2
- 55. Energy 120 J CO2
- 56. Energy 150 J CO2
- 57. Energy 150 J CO2
- 58. Energy 150 J CO2
- 62. Pressors Mader (2008) Resuscitation
- 65. Ventilation? Kern (2002) Circulation
- 66. Ventilation Sigurdsson et al (2003) Curr Opin Crit Care
- 67. Continuous Chest Compressions with Synchronous Ventilations (10:1)
- 68. Bag-Valve-Mask
- 71. Priming the Pump
- 73. Priming the Pump Holzer (2004) Anesth Analg
- 74. Clear? <3 sec 6.7 Odds <6 sec 10.7 Odds Shock Both 13.1 Odds
- 75. Clear?
- 78. Secondary VF
- 84. Hypocapneic Vasoconstriction Idris (in preparation)
- 85. Cerebral Perfusion During Shock P = .004 v 12 P = .004 v 12 mL/100 gm/min
- 86. Brain Oxygenation During Shock P = .0016 vs 12 P = .0046 vs 12 mm Hg
- 87. EtCO2 & Cerebral Perfusion
- 89. Rapid, Shallow Breaths? Davis (in preparation)
- 90. Intrathoracic Pressure Davis (in preparation)
- 91. Hyperventilation Davis, Bulger (2005-08) Crit Care Med, J Trauma
- 92. Why should we cool?
- 94. Evidence for Hypothermia Hypothermia After Cardiac Arrest Study Group (2002) NEJM
- 95. Who should we cool?
- 96. Early Hypothermia Abella (2004) Circulation
- 97. Prehospital Hypothermia Kim (2007) Circulation
- 99. It’s not the fall… It’s the landing!
- 100. CO 2 ATP 3 Na + 2 K + ATP O 2 Glucose X Ischemia/Reperfusion ROS
- 101. Hyperoxia?
- 102. Hyperoxia? Davis (2010) Neurotrauma
- 105. Objective: To Cheat This Man!
- 110. Circulation
- 112. Ventilation
- 113. Ventilation
- 115. Shark Hook?
- 116. Shark Hook?
- 117. Baseline (13:51)
- 118. Baseline (13:51)
- 119. Seizure (14:03)
- 120. Seizure (14:03)
- 121. Postictal with Inspiratory Stridor (14:06)
- 122. Postictal with Inspiratory Stridor (14:06)
- 123. Desaturating (14:13)
- 125. Bigeminy (14:24)
- 126. Airway Management (14:44 to 14:48)
- 127. Clinical Course ST Elevation SpO2 HR SBP
- 130. Positioning
- 131. Positioning Rolls onto side
- 135. UCSD Center for Resuscitation Science People should not die before they are done living.
Editor's Notes
- This animal model demonstrates why current CPR protocols are inadequate. This represents “perfect” CPR by current standards – machine-driven CPR from the moment the switch is flipped with perfect rate and depth and an optimal compression:ventilation ratio of 15:2. It is worth noting that the pauses for ventilation here are much shorter than in “real life” CPR, whether by laypersons or professionals, which only magnifies the problems seen here. Graphed in the background are aortic and RA pressures – the two components of CPP. Observe that it takes the entire cycle of chest compressions before the threshold for CPP is reached (represented by the horizontal line). Once this value is obtained, there are only a few compressions left before a pause for ventilation. The decline in aortic pressure is even faster than the gradual rise. This would suggest that standard “optimal” CPR will never adequately prime the heart.
- This animal model demonstrates why current CPR protocols are inadequate. This represents “perfect” CPR by current standards – machine-driven CPR from the moment the switch is flipped with perfect rate and depth and an optimal compression:ventilation ratio of 15:2. It is worth noting that the pauses for ventilation here are much shorter than in “real life” CPR, whether by laypersons or professionals, which only magnifies the problems seen here. Graphed in the background are aortic and RA pressures – the two components of CPP. Observe that it takes the entire cycle of chest compressions before the threshold for CPP is reached (represented by the horizontal line). Once this value is obtained, there are only a few compressions left before a pause for ventilation. The decline in aortic pressure is even faster than the gradual rise. This would suggest that standard “optimal” CPR will never adequately prime the heart.
- These data are from the SD Trauma Registry and suggest an optimal arrival pCO2 range, with both hyper- and hypoventilation leading to poor outcomes. The adjusted odds ratios take into account the following: age, gender, mechanism, Head AIS, ISS, GCS, hypotension, and base deficit.
- This animal model demonstrates why current CPR protocols are inadequate. This represents “perfect” CPR by current standards – machine-driven CPR from the moment the switch is flipped with perfect rate and depth and an optimal compression:ventilation ratio of 15:2. It is worth noting that the pauses for ventilation here are much shorter than in “real life” CPR, whether by laypersons or professionals, which only magnifies the problems seen here. Graphed in the background are aortic and RA pressures – the two components of CPP. Observe that it takes the entire cycle of chest compressions before the threshold for CPP is reached (represented by the horizontal line). Once this value is obtained, there are only a few compressions left before a pause for ventilation. The decline in aortic pressure is even faster than the gradual rise. This would suggest that standard “optimal” CPR will never adequately prime the heart.
- This animal model demonstrates why current CPR protocols are inadequate. This represents “perfect” CPR by current standards – machine-driven CPR from the moment the switch is flipped with perfect rate and depth and an optimal compression:ventilation ratio of 15:2. It is worth noting that the pauses for ventilation here are much shorter than in “real life” CPR, whether by laypersons or professionals, which only magnifies the problems seen here. Graphed in the background are aortic and RA pressures – the two components of CPP. Observe that it takes the entire cycle of chest compressions before the threshold for CPP is reached (represented by the horizontal line). Once this value is obtained, there are only a few compressions left before a pause for ventilation. The decline in aortic pressure is even faster than the gradual rise. This would suggest that standard “optimal” CPR will never adequately prime the heart.
- This animal model demonstrates why current CPR protocols are inadequate. This represents “perfect” CPR by current standards – machine-driven CPR from the moment the switch is flipped with perfect rate and depth and an optimal compression:ventilation ratio of 15:2. It is worth noting that the pauses for ventilation here are much shorter than in “real life” CPR, whether by laypersons or professionals, which only magnifies the problems seen here. Graphed in the background are aortic and RA pressures – the two components of CPP. Observe that it takes the entire cycle of chest compressions before the threshold for CPP is reached (represented by the horizontal line). Once this value is obtained, there are only a few compressions left before a pause for ventilation. The decline in aortic pressure is even faster than the gradual rise. This would suggest that standard “optimal” CPR will never adequately prime the heart.
- This demonstrates the importance of recoil, with good CPR on the top (although its worth pointing out that the ventilation rate is too fast) as evidenced by a negative intrathoracic pressure with each cycle, and bad CPR on the bottom with continuous positive intrathoracic pressure due to incomplete recoil.
- This demonstrates the importance of recoil, with good CPR on the top (although its worth pointing out that the ventilation rate is too fast) as evidenced by a negative intrathoracic pressure with each cycle, and bad CPR on the bottom with continuous positive intrathoracic pressure due to incomplete recoil.
- This animal model demonstrates why current CPR protocols are inadequate. This represents “perfect” CPR by current standards – machine-driven CPR from the moment the switch is flipped with perfect rate and depth and an optimal compression:ventilation ratio of 15:2. It is worth noting that the pauses for ventilation here are much shorter than in “real life” CPR, whether by laypersons or professionals, which only magnifies the problems seen here. Graphed in the background are aortic and RA pressures – the two components of CPP. Observe that it takes the entire cycle of chest compressions before the threshold for CPP is reached (represented by the horizontal line). Once this value is obtained, there are only a few compressions left before a pause for ventilation. The decline in aortic pressure is even faster than the gradual rise. This would suggest that standard “optimal” CPR will never adequately prime the heart.
- This animal model demonstrates why current CPR protocols are inadequate. This represents “perfect” CPR by current standards – machine-driven CPR from the moment the switch is flipped with perfect rate and depth and an optimal compression:ventilation ratio of 15:2. It is worth noting that the pauses for ventilation here are much shorter than in “real life” CPR, whether by laypersons or professionals, which only magnifies the problems seen here. Graphed in the background are aortic and RA pressures – the two components of CPP. Observe that it takes the entire cycle of chest compressions before the threshold for CPP is reached (represented by the horizontal line). Once this value is obtained, there are only a few compressions left before a pause for ventilation. The decline in aortic pressure is even faster than the gradual rise. This would suggest that standard “optimal” CPR will never adequately prime the heart.
- This animal model demonstrates why current CPR protocols are inadequate. This represents “perfect” CPR by current standards – machine-driven CPR from the moment the switch is flipped with perfect rate and depth and an optimal compression:ventilation ratio of 15:2. It is worth noting that the pauses for ventilation here are much shorter than in “real life” CPR, whether by laypersons or professionals, which only magnifies the problems seen here. Graphed in the background are aortic and RA pressures – the two components of CPP. Observe that it takes the entire cycle of chest compressions before the threshold for CPP is reached (represented by the horizontal line). Once this value is obtained, there are only a few compressions left before a pause for ventilation. The decline in aortic pressure is even faster than the gradual rise. This would suggest that standard “optimal” CPR will never adequately prime the heart.
- These animal data suggest that part of the detrimental effect of overventilation may be immunologic and that this effect is most profound within the first 2 hours of injury.
- This demonstrates the importance of recoil, with good CPR on the top (although its worth pointing out that the ventilation rate is too fast) as evidenced by a negative intrathoracic pressure with each cycle, and bad CPR on the bottom with continuous positive intrathoracic pressure due to incomplete recoil.
- These VF tracings demonstrate the priming effect from an electrophysiological perspective. As pointed out with the 3-phase model schematic, the morphology of VF changes as time passed. The VF at 1 min is well within the electrical phase, with greater amplitude and median frequency. After 8 min, the morphology is very different; a shock at this point would likely be unsuccessful in producing ROSC. However, after only 90 sec of chest compressions, the morphology looks similar to the “fresh” VF on the left. It is worth pointing out that the experimental model for producing PEA is to induce VF, wait 8 min, and shock without antecedent chest compressions – exactly what many EMS systems would currently advocate. This issue will resurface when we discuss the control group for the CPR timing study.
- These VF tracings demonstrate the priming effect from an electrophysiological perspective. As pointed out with the 3-phase model schematic, the morphology of VF changes as time passed. The VF at 1 min is well within the electrical phase, with greater amplitude and median frequency. After 8 min, the morphology is very different; a shock at this point would likely be unsuccessful in producing ROSC. However, after only 90 sec of chest compressions, the morphology looks similar to the “fresh” VF on the left. It is worth pointing out that the experimental model for producing PEA is to induce VF, wait 8 min, and shock without antecedent chest compressions – exactly what many EMS systems would currently advocate. This issue will resurface when we discuss the control group for the CPR timing study.
- These VF tracings demonstrate the priming effect from an electrophysiological perspective. As pointed out with the 3-phase model schematic, the morphology of VF changes as time passed. The VF at 1 min is well within the electrical phase, with greater amplitude and median frequency. After 8 min, the morphology is very different; a shock at this point would likely be unsuccessful in producing ROSC. However, after only 90 sec of chest compressions, the morphology looks similar to the “fresh” VF on the left. It is worth pointing out that the experimental model for producing PEA is to induce VF, wait 8 min, and shock without antecedent chest compressions – exactly what many EMS systems would currently advocate. This issue will resurface when we discuss the control group for the CPR timing study.
- These data are from the SD Trauma Registry and suggest an optimal arrival pCO2 range, with both hyper- and hypoventilation leading to poor outcomes. The adjusted odds ratios take into account the following: age, gender, mechanism, Head AIS, ISS, GCS, hypotension, and base deficit.
- This graph demonstrates the importance of the lowest and final end-tidal CO2 values in predicting mortality – much more important than any of the oxygenation measures.
- This graph demonstrates the importance of the lowest and final end-tidal CO2 values in predicting mortality – much more important than any of the oxygenation measures.
- This graph demonstrates the importance of the lowest and final end-tidal CO2 values in predicting mortality – much more important than any of the oxygenation measures.
- This animal model demonstrates why current CPR protocols are inadequate. This represents “perfect” CPR by current standards – machine-driven CPR from the moment the switch is flipped with perfect rate and depth and an optimal compression:ventilation ratio of 15:2. It is worth noting that the pauses for ventilation here are much shorter than in “real life” CPR, whether by laypersons or professionals, which only magnifies the problems seen here. Graphed in the background are aortic and RA pressures – the two components of CPP. Observe that it takes the entire cycle of chest compressions before the threshold for CPP is reached (represented by the horizontal line). Once this value is obtained, there are only a few compressions left before a pause for ventilation. The decline in aortic pressure is even faster than the gradual rise. This would suggest that standard “optimal” CPR will never adequately prime the heart.
- This animal model demonstrates why current CPR protocols are inadequate. This represents “perfect” CPR by current standards – machine-driven CPR from the moment the switch is flipped with perfect rate and depth and an optimal compression:ventilation ratio of 15:2. It is worth noting that the pauses for ventilation here are much shorter than in “real life” CPR, whether by laypersons or professionals, which only magnifies the problems seen here. Graphed in the background are aortic and RA pressures – the two components of CPP. Observe that it takes the entire cycle of chest compressions before the threshold for CPP is reached (represented by the horizontal line). Once this value is obtained, there are only a few compressions left before a pause for ventilation. The decline in aortic pressure is even faster than the gradual rise. This would suggest that standard “optimal” CPR will never adequately prime the heart.