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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, MDUCSD Center for Resuscitation Science ART: A New Model of Resuscitation
- 2. Goals To convinceyou that: Training affects performance Performance affects outcomes
- 3. Objectives What isART? Seven commandments of cardiac arrest Post-arrest care Pre-arrest care Sample patient flow diagrams Skills training
- 4. UCSD Center forResuscitation Science People should not die before they are done living.
- 5. Our Mission Toprevent the preventable To resuscitate the resuscitatable To recognize the futile
- 6. Elevated life supporttraining from a regulatory requirement into the primary vehicle for addressing all resuscitation-related issues.
- 7. ART Model Scaffoldingfor resuscitation program Flexible, adaptive training Integrated curriculum Agency-specific algorithm, equipment Cognitive psychology Expert instructors Competency assessments & CQI data
- 8.
- 9.
- 10. Integrated Critical CareModel PART BART ART HeART TART RAT AART PhART
- 11.
- 12.
- 13.
- 14.
- 15.
- 16.
- 17.
- 18.
- 19. ART responsible formore than 85% of the decrease! Overall Impact
- 20.
- 21.
- 22. San Diego EMSBaseline Training #1 Training #2
- 23. El Cajon CardiacArrests 1.6% Survival 9.0% Survival Cogntiive training
- 24. Confirm ETCO2 EDDBreath sounds SaO2 Maximize 1 st Attempt Prevent Hypoxic Arrest Overall Intubation Success BVM 1 until return of spontaneous respirations SaO2<94% Obstructed SaO2 94% Anterior Anticipate problem Traumatized Unsuccessful 5 Successful Successful Abandon attempt 3 SaO2 94% “ Can’t intubate, can oxygenate” SaO2<94% “ Can’t intubate, can’t oxygenate” Can maintain SaO2 ~90% Can’t maintain SaO2 ~90% Successful Unsuccessful Unable intubate Unsuccessful Successful 1 Tight seal, jaw thrust, Sellick maneuver, NPA/OPA 2 Look, External (3-3-2), Mallampati, Obstruction, Neck (manual ILS) 3 SaO2 dropping below 95%, clearly unable to intubate, bradycardia 4 May not work with upper airway obstruction; may need to adjust position 5 Consider repeating etomidate/succinylcholine Normal Able to intubate NRB 1-3” Preoxygenate with NRB BVM 1 Preload bougie Access cric kit Consider Miller Sellick Sedative Paralytic SaO2 94% BVM 1 1 st Look External laryngeal manipulation (ELM) BVM 1 (Consider other intubator or immediate transport) SaO2 <94% Bougie ELM Miller blade Suction/Magills Bougie Cricothyrotomy Rapid Airway Access Combitube/LMA 4 Cricothyrotomy Other intubator (OTI/bougie) Pre-assessment (LEMON) 2 Suction Combitube/ LMA 4 Cricothyrotomy 1 st Attempt
- 25.
- 26. Airway Management PreoxygenationApproach
- 27.
- 28. Traumatic Brain Injury83.3% 80.6% 78.5%
- 29.
- 30.
- 31. Commandment I Arrestvictims should have high quality compressions performed from the moment of arrest until ROSC is assured.
- 32. Prime the Pump!Kern (2002) Circulation
- 33. Stay on thechest! Christenson (2009) Circulation * Adjusted for: age, gender, bystander CPR, public location, response time, compression rate
- 34. Codus Interruptus Initiatingcompressions Rhythm analysis Shock sequence Pulse check Intubation Vascular access
- 35.
- 36. Stiell et al(2008) AHA Scientific Sessions Deeper Compressions
- 37. Aufderheide (2005) Resuscitation Recoil?
- 38.
- 39. Results Chest compressionfraction 91% Compression rate 123/min Compression depth 2.6 inches Pre-shock pause 2.6 sec Post-shock pause 3.6 sec Perfusion check 4.3 sec Ventilation rate 9.7/min PetCO2 15.3 mmHg
- 40.
- 41. Return of SpontaneousCirculation Electrical (HR) Mechanical (PetCO2)
- 42. Lung Perfusion inShock
- 43. PaCO2 40 mmHgPetCO2 37 mmHg 40 40 40 40 40 40
- 44. PaCO2 40 mmHgPetCO2 23 mmHg 0 40 40 40 0 40
- 45. PaCO2 40 mmHgPetCO2 11 mmHg 0 40 0 40 0 0
- 46.
- 47. 53 y/o femalevisiting San Diego with husband Riding in Pedi-Cab downtown Turns too sharply, flips over Patient strikes occiput on curb with immediate loss-of-consciousness Case
- 48.
- 49. Paramedics find patientobtunded SBP 160, HR 75, agonal respirations, GCS 3 BVM ventilations initiated Spinal precautions, IV started, monitoring Case
- 50. HR decr to27 “Cushing’s response” Unable to get SpO2 reading Proceeded with ETI protocol Unable to obtain PetCO2 reading x 2 monitors Return to BVM ventilation ED – GCS 3, apnea, HR 23, SpO2 UTO Case
- 51. Chest compressions startedPetCO2 to 13 mmHg Good recoil from compressions PetCO2 to 19 mmHg Vasopressin 40u IV, epinephrine 1mg IV HR to 110 PetCO2 to 37 mmHg Case
- 52. Compression pause forperfusion check No palpable femoral pulses PetCO2 35-38 mmHg Compressions restarted, then stopped Trauma attending confirmed palpable femoral pulse CT head revealed nonsurvivable TBI Multi-organ donor Case
- 53. ROSC Predictors HREtCO2
- 54.
- 55. Energy 120 JCO2
- 56. Energy 150 JCO2
- 57. Energy 150 JCO2
- 58. Energy 150 JCO2
- 59.
- 60.
- 61. Commandment II Pressorsaugment compressions.
- 62. Pressors Mader (2008) Resuscitation
- 63.
- 64. Commandment III Ventilations(10:1 synchronous) provide oxygenation for prolonged or non-VF arrests.
- 65. Ventilation? Kern (2002) Circulation
- 66. Ventilation Sigurdsson etal (2003) Curr Opin Crit Care
- 67. Continuous Chest Compressions with Synchronous Ventilations (10:1)
- 68.
- 69.
- 70. Commandment IV Compressions(with a pressor) should precede all shocks except the initial shocks in a monitored VF/VT arrest.
- 71.
- 72.
- 73. Priming the PumpHolzer (2004) Anesth Analg
- 74. Clear? <3 sec6.7 Odds <6 sec 10.7 Odds Shock Both 13.1 Odds
- 75.
- 76.
- 77.
- 78.
- 79.
- 80. Commandment V Searchfor a reversible cause of arrest.
- 81.
- 82. Commandment VI Controlventilation, support hemodynamics, decrease FiO2 and consider hypothermia after ROSC.
- 83.
- 84. Hypocapneic Vasoconstriction Idris(in preparation)
- 85. Cerebral Perfusion DuringShock P = .004 v 12 P = .004 v 12 mL/100 gm/min
- 86. Brain Oxygenation DuringShock P = .0016 vs 12 P = .0046 vs 12 mm Hg
- 87. EtCO2 & CerebralPerfusion
- 88.
- 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 wecool?
- 93.
- 94. Evidence for HypothermiaHypothermia After Cardiac Arrest Study Group (2002) NEJM
- 95. Who should wecool?
- 96. Early Hypothermia Abella(2004) Circulation
- 97. Prehospital Hypothermia Kim(2007) Circulation
- 98.
- 99. It’s not thefall… It’s the landing!
- 100. CO 2 ATP3 Na + 2 K + ATP O 2 Glucose X Ischemia/Reperfusion ROS
- 101.
- 102. Hyperoxia? Davis (2010) Neurotrauma
- 103.
- 104. Commandment VII Preventionbeats resuscitation every time.
- 105. Objective: To CheatThis Man!
- 106.
- 107.
- 108.
- 109. Rapid Response CriteriaRespiratory Respiratory distress Hypoxemia Hypercapnia Work of breathing Tachypnea Infectious Fever Clinical Intuition Intuitive sense that something is wrong Circulation Hypoperfusion Tachycardia Hypotension Others Neurologic Change in mental status New neurological deficits
- 110.
- 111. Circulation Treatment PositioningSupine IV Fluids Bolus, maintenance Pressors Inotropes Vasoconstrictors Codes STEMI SEPSIS Blue (CPR) Triggers Chief complaint CP, SOB Vitals/exam BP, HR Mental status Temp Laboratory/monitor Lactate, BD, bicarb ST elev PVC’s/Vtach CVP, CO, SVR
- 112.
- 113.
- 114. Ventilation Treatment PositioningUpright Oxygen NC, NRB NPA, OPA Medications Bronchodilators CHF treatment Ventilatory support BVM assist, BiPAP Intubation Triggers Chief complaint SOB Vitals/exam Work of breathing RR, SpO 2 Mental status Temp Laboratory/monitor ABG EtCO 2 PVC’s/Vtach
- 115.
- 116.
- 117.
- 118.
- 119.
- 120.
- 121. Postictal with InspiratoryStridor (14:06)
- 122. Postictal with InspiratoryStridor (14:06)
- 123.
- 124.
- 125.
- 126. Airway Management (14:44to 14:48)
- 127. Clinical Course STElevation SpO2 HR SBP
- 128. Clinical Course Ruledin for MI Troponins, EKG evolution Echo with moderate global hypokinesis Repeat unchanged Cath = no coronary artery disease
- 129.
- 130.
- 131.
- 132.
- 133.
- 134. Helpful Hints Impartenthusiasm and hope! Part of something big and exciting Be an expert…or at least invoke one Cognitive psychology Makes “BLS before ALS” more exciting Continually reference algorithm Admit that we don’t know everything
- 135. UCSD Center forResuscitation Science People should not die before they are done living.
Editor's Notes
- #12 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.
- #21 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.
- #29 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.
- #33 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.
- #34 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.
- #36 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.
- #37 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.
- #38 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.
- #39 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.
- #63 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.
- #66 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.
- #67 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.
- #68 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.
- #72 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.
- #74 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.
- #79 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.
- #92 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.
- #100 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.
- #102 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.
- #103 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.
- #107 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.
- #108 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.