Resuscitation  what works  what doesnt and whats coming down the tube    persoff
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Resuscitation  what works  what doesnt and whats coming down the tube    persoff Resuscitation what works what doesnt and whats coming down the tube persoff Document Transcript

  • Resuscitation: What Works, What Doesn’t, and What’s Coming Down the Tube Jason Persoff, M.D., S.F.H.M. ©2010 MFMER | slide-1Financial DisclosuresNone to reportMotivational Disclosures ©2010 MFMER | slide-2
  • Explain the Gorilla Again…• How much time did that video take? • Exactly 82 seconds• In the hospital, how long does it take to recognize cardiac arrest? Herlitz et al. Resuscitation 2001.
  • Are We Sure He’s Dead, Jim?• Eberle confirmed our skills at pulse check • Sensitivity 90% • Specificity 55% • Accuracy 65% • Median time needed to identify presence or absence of pulse: • 24 seconds overall, 32 seconds for pulse absent patients• In 2009, Tibbells confirmed we’d only gotten a little better • Sensitivity 86% • Specificity 64% • Accuracy 78%• Bottom line: in controlled circumstances, we don’t know if a patient has a pulse or not Eberle et al. Resuscitation 1996 (33) Tibballs J and Russell Philip. Resuscitation 2009; 80: 61Clinically Futile Cycles• Pulse Check• Rhythm Analysis• Failure to Simulate, Rehearse, React • “…the typical cardiac arrest victim receives a faster response as a casino patron than they do as a hospital inpatient.” • Adams BA, et al. Resuscitation 2009; 80: 65.
  • New BCLS Guidelines Emphasize What Works
  • Cerebral Performance Category Neurologically Intact Survival (CPC 0-1) CPC Status Survival to Hospital Discharge •0 Normal •1 Good •2 Mod DisabilityReturn of Spontaneous Circulation •3 Major Disability •4 Persistent Vegetative State •Brain Death Death 88% of all In-Hospital Cardiac Arrests Occur on Patients with DNR Status Hodgetts et al. Resuscitation 54: 2002
  • Outcomes in VF / VT Total Surviving Neurologically Intact ~12% Neurologically Intact Survival 58-75% CPC (CPC 0-1) Status Survival to Hospital Discharge 17-57% •0 Normal •1 Good 54-76% •2 Mod DisabilityReturn of Spontaneous Circulation •3 Major Disability •4 Persistent Vegetative State •Brain Death Death 14-27% of Pediatric In-Hospital Arrests 24% of Adult In-Hospital Arrests Samson et al. NEJM 354: 2006 Nadkarni, et al. JAMA 295: 2006 Outcomes in PEA / Asystole Total Surviving Neurologically Intact ~6.8% Neurologically Intact Survival 61-62% CPC (CPC 0-1) Status Survival to Hospital Discharge 10-20% •0 Normal •1 Good 53-52% •2 Mod DisabilityReturn of Spontaneous Circulation •3 Major Disability •4 Persistent Vegetative State •Brain Death Death Usually preceded up to 8 hours prior to arrest by marked changes in SBP, HR, or oxygen saturation Skrifvars et al. Resuscitation 70: 2006 Nadkarni, et al. JAMA 295: 2006
  • Cardiac Arrest Physiology Untreated V-Fib/VT After Mader T, Resuscitation 2007 Electrical Phase Metabolic Phase Circulatory Phase 0-4 minutes 4-10 minutes 10+ minutes High Countershock CPR Needed Before Comprehensive Receptivity Shock Multisystem Approach Losing Time, Losing Life Circulatory Metabolic Acute VF Electrical Arrest Phase Phase Fibrillating myocardium Phase deplete of ATP Weisfeldt ML and Becher LB. JAMA 2002; 288: 3035.Circulatory Code Team CPR, Drugs, Code Team Collapse Arrival Intubation Begins to 0-3 Mins 3-6 Mins 6-10 Mins Integrate 10+ Mins •Pulse Check? •How quickly does •Arrhythmia •Call Code? the team arrive Recognition? and who leads? •Airway, Breathing •Kitchen Sink •CPR? •Txfr or •Shocks •Drugs Pronounced
  • Decreased Survival Predictable Survival ↓ 34% to 14% Herlitz et al. CPR Initiated Quality of Resuscitation Lots o’ Stuff 49: 2001 >1-2 Minutes CPR After Collapse Cooper et al. Resuscitation 68: 2006 SHD Survival ↓ 31% vs. 20% Starts @ 2Mins 30 daySurvival 0% Code Team ACLS 26% vs. 5.9% @ 6 Mins Arrival > 3 Training 1 yearSkrifvars et al. Minutes After Status of 21% vs. 0%Resuscitation Collapse Nurses 70: 2006 Moretti et al. Resuscitation 72: 2007 Compressions Matter Pump Fast Push Good Hard Recoil Chest Compressions CPR when done perfectly provides only… Start –1/3 normal cardiac Now output –10-15% normal cerebral blood flow –1-5% normal cardiac blood flow Sanders et al. Resuscitation 1985.
  • Compressions Matter• Compressions too shallow 62.6% of the time• Compressions too slow 71.9% of the time ROSC No ROSC Quartile 1 95.5 - 138.7 cpm 75% 25% * Quartile 2 76% 24% * 87.1 – 94.8 cpm Quartile 3 58% 42% * * p < 0 .0083 72.4 – 87.1 cpm Quartile 4 42% 58% * 40.3 – 72.0 cpm Abella. Circulation 2005; 111:428-34Compressions Matter % 42% Incomplete Release % 0% Too Deep % 62% Too Shallow 0% 20% 40% 60% 80% Wik et al. JAMA 2005: 293:299-304
  • The Hands Off Interval Yu et al. Circulation 2002; 106:368-72
  • Physiologic ConsequencesPhysiologic Consequences • Compression depth inversely correlates with likelihood of successful defibrillation • Mechanisms of why this may happen • Rapid drops in aortic diastolic pressure • Expansion of the right heart (compromising left ventricular size and flow) • Delays in resuming chest compressions following defibrillation decrease ROSC and neurological intact survival Edelson DP, et al. Resuscitation 2006; 71: 137. Yu et al. Circulation 2002; 106: 368. Chamberlain D, et al. Resuscitation 2008; 77: 10. Berg RA, et al. Resuscitation 2008; 78: 71.
  • Shock ‘Em• AEDs • Widely available but with long hands-off times• Shock ‘Em NOW! Chan PS, et al. NEJM 2008; 358: 9. Lloyd MS, et al. Circulation 2008; 117: 2510. Op Ed: Perkins GD. Resuscitation 2008; 79: 1.Shock ‘em Yesterday• Risk of shock: negligible • Brave volunteers didn’t die • Few case reports Op Ed: Perkins GD. Resuscitation 2008; 79: 1.
  • Er…I Can’t Check The Rhythm Due toCompressions…So…Hands Off, Right?• Wrong…Zoll (among other manufacturers have accelerometer pads that “zero out” compressions
  • Shocking • Delayed defibrillation • Black race associated with delays in defibrillation (p<0.001) • Small hospital size (<250 beds) • “After hours” (nights/weekends) • Non-monitored bed Chan PS, et al. NEJM 2008; 358: 9. Herlitz et al. Resuscitation 2001.So If We Can’t Check A Pulse…?• Continuous capnography • Increasingly appears to be predictive of excellent perfusion • Markers of perfusion include a sudden increase in PCO2 • Ventilations can be titrated to accommodate for EtCO2 of 35-40mmHg
  • Whatever Happened to the ABC’s?Oxygen is CO2 Rapidly Rapidly Rises Hypoxia HypercarbiaConsumed •Adds to acid burden •Needs lung perfusion •2-4 Minutes and ventilation to •Asymmetric clear distribution “The Drain” Switch toAnaerobic Low FlowMetabolism •Functional reductions Lactic Circulatory in compression-•Hepatic perfusion Acidosis Collapse assisted forward flownecessary to clear •Arteriole failure with•pKa, pH and other low effective blood changes change volumesmedication effects
  • New Paradigm: CCR• “Iatrogenic hypotension” – Over-zealous BVM use due to • Desire to correct hypoxia • Belief that hyperventilation will correct acid-base derangements• What is the appropriate tidal volume for a patient in cardiopulmonary arrest? • Roughly 750cc• What is the volume of an adult bag-valve- mask? • 1.5 liters • Designed for 1-handed operationNew Paradigm: CCR Michard F. Anesthesiology 2005
  • New Paradigm: CCR• Phenomenon of auto-PEEP usually referred to patients on a ventilatorNew Paradigm: CCR• Rate exceeded at least 60.9% of the time in humans• In swine models, hyperventilation results in… • …increased intrathoracic pressure • …decreased coronary perfusion pressures • …lower survival •Abella. Circulation 2005; 111:428-34. • Aufderheide, et al. Resuscitation 2004.
  • Oral AirwaysOral Airways• Contraindicated in conscious patients • Can premote retching and laryngospasm • Trauma
  • Why is Airway De-Emphasized? • Patients gasp during cardiac arrest • Gasping… • …is a forceful agonal respiration • …is a marker of improved prognosis • …increases cerebral blood flow • …decreases intracranial pressure • …improves upper airway patency • …generates cardiac output •Yang, et al. Crit Care Med 1994; 22: 879. •Ristagno G, et al. Resuscitation 2007; 75: 366. •Xie J, et al. Crit Care Med 2004; 32:238. •Srinivasan V, et al. Resuscitation 2006; 69: 329. •Ewy GA and Kern KB. J Am Coll of Cardiol 2009; 53:147. GASP!!!! Rats! A hemorrhagicmodel of PEA in rats Suzuki M, et al. Resuscitation 2009; 80:109.
  • External Cooling
  • Cold Is Cool• Why hypothermia? • Superoxide generation post-resuscitation • Calcium influx into cells • Decreased available glucose • Increased oxidative phosphorylation • Cooling preserves mitochondria • The only “brain preserving” therapy post-arrest• Hazards • Coagulopathy • Impaired WBC function • Decrease in cardiac index • Hyperglycemia (Real)• Requires • Continuous bladder or central monitoring of temperature • Target 32-34°CCold is CoolA. Aguila et al. / Resuscitation81 (2010) 1621–1626
  • Cold is Cool70%60%50%40% Hypothermia30% Normothermia20%10%0% Good Neuro Bad Neuro Death After data from SA Bernard, et al. NEJM 2002; 346: 557-63. Cold is Cool 60% 50% 40% 30% Hypothermia Normothermia 20% 10% 0% Good Neuro Death After data from THACASG. NEJM 2002; 346: 549-56.
  • Cold is Cool After THACASG. NEJM 2002; 346: 549-56.Cold Is Cool• Therapeutic Hypothermia • Depression in cardiac index from TH means pressors are indicated • Maintenance of MAP 90-100mmHg • Oddo M, et al. Crit Care Med 2006 • Paralysis is recommended but must be combined with sedation • Paralysis is stopped once core temp is >35°C • TH causes selective increases in CK-MB • Standard resuscitation peak ~100 at 6 hrs • TH resuscitation peak ~300 at 12 hrs • Nevertheless, STEMI or suspicion of MI should NOT preclude PCI
  • Cold Is Cool• Therapeutic Hypothermia • Goal: RAPID decrease in core temp to 32-34 Deg C • Average 6 hours to achieve targets • Oddo M, et al. Crit Care Med 2006 • Cold LR 30mL/kg bolus plus external cooling in comatose patients post- resuscitation • Bottom Line: HIGHER CPC SCORES, SIMILAR SURVIVAL • CPC 0-1 seen in 54% of those treated vs. 30% of controls • Review: Bro-Jeppensen J, et al. Resuscitation 2009; 80: 171. • Theoretical decrease in diminishment of ECG VF to asystole • Cooling DURING arrest seems to improve ROSC, but not survival • Pre-Arrest and Intra-Arrest Hypothermia and VF. Menegazzi JJ, et al. Resuscitation 2009; 80: 126.Fin
  • Universal Algorithm Yep Nope V-Fib Shockable Rhythm? PEA Pulseless VT Asystole Have no idea 360J Antiarrhythmic Mono (Amiodarone) or Shock 150J Biphasic Drug Biphasic Shock 150J 5 Cycles (150 Compressions) Pressor (Epi vs. Vaso) Assignment #1• You come across an unconscious patient who appears unarousable and not particularly lively. As a group, determine: • Who will lead the code • Determine interventions prior to defibrillator arrival • When the defibrillator arrives, how would you set it up?
  • Debriefing #1• Group leader, discuss what chaos ensued• How did you figure out to use the defibrillator?• How did you decide on a collective course of action?• What areas of uncertainty existed?• Take 2: new group leader, same exerciseVF/Pulseless VT• Peripheral vs. Central Lines• Precordial Thumps• Cough CPR• Pulse Checks
  • Universal Algorithm Yep Nope V-Fib Shockable Rhythm? PEA Pulseless VT Asystole Have no idea 360J Antiarrhythmic Mono (Amiodarone) or Shock 150J Biphasic Drug Biphasic Shock 150J 5 Cycles (150 Compressions) Pressor (Epi vs. Vaso) PEA: A Common Cause of Arrest Desbiens NA, Crit Care Med 2008; 36:391.
  • PEA: A Common Cause of Arrest• All patients in PEA should receive: • IVF wide open to “fill the tank” • Patients will go into vascular collapse commonly as shock ensues increasing the relative vascular volume by many liters • Oxygen • Systemic hypoxia causes vasoconstriction of the pulmonary arteries leading to RV dysfunction and thus decreases in LV preload • Epinephrine • Peripheral alpha-agonist can clamp down the vessels effectively but will also increase myocardial workload via beta-agonist effects. This is a short-term fix • Chest Compressions • Already discussed Assignment #2• Your team arrives on a patient who is agonally breathing but appears to have a very faint, rapid pulse. • At what point would you institute chest compressions? • What interventions should you initiate immediately and why? • Name some immediate causes that could have led to this collapse
  • Debrief #2• What were the difficulties this go around in deciding course of action?• Ultimately, what did your group decide was the etiology for the collapse and how did you approach it?• What algorithms do you think may have helped you perform better?Bradycardia
  • Tachycardia What, No Love for CCR?• Effect of CCR on Alveolar Collapse and Recruitment • More Atelectasis • More Hypoxemia • Worse Hemodynamics • Effects Persist Even After Resumption of IPPV • But…the pigs used were anesthetized • Markstaller K, et al. Resuscitation 2008; 79: 125.
  • Resuscitation Medications Epinephrine Vasopressin Epinephrine Steroids plus Vasopressin Sillberg VAH, et al. Methyl- Resuscitation Sillberg VAH, et al. Prednisolone 40mg 2008; 79: 380. Resuscitation IV afterSillberg VAH, et al. 2008; 79: 380. Resuscitation Epinephrine Wyer, et al. Ann 2008; 79: 380. Yup in animals, not Emergency Med Hydrocortisone 2006; 48: 86. so in humans 300mg qd x 7 days largely due to Koshman, et al. study design Mentzelopoulos SD, Ann of heterogeneity. et al. Arch Int Med Pharmacology 2009; 169: 15. 2005; 39: 1687. α/β Agonist β Non-Adrenergic Smoke if You Got Low Relative Vasoconstrictor ‘Em Cortisol Levels External Cooling
  • Cold Is Cool• Why hypothermia? • Superoxide generation post-resuscitation • Calcium influx into cells • Decreased available glucose • Increased oxidative phosphorylation • Cooling preserves mitochondria • The only “brain preserving” therapy post-arrest• Hazards • Coagulopathy • Impaired WBC function • Decrease in cardiac index • Hyperglycemia (Real)• Requires • Continuous bladder or central monitoring of temperature • Target 32-34°C Cold is Cool 70% 60% 50% 40% Hypothermia 30% Normothermia 20% 10% 0% Good Neuro Bad Neuro Death After data from SA Bernard, et al. NEJM 2002; 346: 557-63.
  • Cold is Cool 60% 50% 40% 30% Hypothermia Normothermia 20% 10% 0% Good Neuro Death After data from THACASG. NEJM 2002; 346: 549-56.Cold is Cool After THACASG. NEJM 2002; 346: 549-56.
  • Cold Is Cool• Therapeutic Hypothermia • Depression in cardiac index from TH means pressors are indicated • Maintenance of MAP 90-100mmHg • Oddo M, et al. Crit Care Med 2006 • Paralysis is recommended but must be combined with sedation • Paralysis is stopped once core temp is >35°C • TH causes selective increases in CK-MB • Standard resuscitation peak ~100 at 6 hrs • TH resuscitation peak ~300 at 12 hrs • Nevertheless, STEMI or suspicion of MI should NOT preclude PCICold Is Cool• Therapeutic Hypothermia • Goal: RAPID decrease in core temp to 32-34 Deg C • Average 6 hours to achieve targets • Oddo M, et al. Crit Care Med 2006 • Cold LR 30mL/kg bolus plus external cooling in comatose patients post- resuscitation • Bottom Line: HIGHER CPC SCORES, SIMILAR SURVIVAL • CPC 0-1 seen in 54% of those treated vs. 30% of controls • Review: Bro-Jeppensen J, et al. Resuscitation 2009; 80: 171. • Theoretical decrease in diminishment of ECG VF to asystole • Cooling DURING arrest seems to improve ROSC, but not survival • Pre-Arrest and Intra-Arrest Hypothermia and VF. Menegazzi JJ, et al. Resuscitation 2009; 80: 126.
  • Post-Cardiac Arrest SyndromeRespect for the RRT?• Does an RRT decrease mortality and frequency of codes: Maybe • Yes: Downey AW, et al. Crit Care Med 2008; 36: 477. • Measured alteration in mental status • Delay in MET call resulted in death (37% vs. 22%) • Yes: Dacey MJ, et al. Crit Care Med 2007; 35: 2076. • Yes: Sebat F, et al. Crit Care Med 2007; 35: 2568. • Yes: Sharek PJ, et al. JAMA 2007; 298: 2267. • No: Chan PS, et al. JAMA 2008; 300: 2506. • Single hospital before and after intervention, no differences in mortality, but decrease in ICU admission rate • No: MERIT Study. Crit Care Resusc 2007; 9: 206. • MET not called for >15 mins prior to CA
  • Respect for the RRT• “Why doesn’t anyone call for help?” • Buist M. Crit Care Med 2008; 36: 634.• Implementation of an RRT improves vital sign recording • Chen J, et al. Resuscitation 2009; 80: 35.Break Isn’t Orientation over yet????