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Cardiac Arrest
Beyond the protocol
David Gale 9th January 2019
Acknowledgements
• Emergency medicine cases
• SMACC
• Authors of the relevant papers
• The Resus Room
• Life in the fast lane
• Deranged physiology
• EmCrit
• Zoll
• Uptodate
• ILCOR/ANZCOR/ERC
• RebelEM
• Ambulance NSW
• GSA HEM
1. Different cardiac arrest syndromes
- profound vasoplegia
1. Different cardiac arrest syndromes
- Refractory ventricular fibrillation
Beyond the protocol
1. Different cardiac arrest syndromes
- Refractory ventricular fibrillation
Defibrillation
Dual sequential defibrillation
High energy biphasic defibrillation
Beyond the protocol
Different cardiac arrest syndromes
- Refractory ventricular fibrillation
- Transport
- Mechanical CPR
- PCI centre
- eCPR
2. Mechanical CPR
3. Monitoring in cardiac arrest
3. Monitoring in cardiac arrest
- wavefrom capnography
12 lead ECG
3. Monitoring in cardiac arrest
- arterial lines and haemodynamic directions
4. Haemodynamic targeted CPR
5. CPR induced
consciousness
6. When to consider pacing in cardiac arrest?
7. Changing thoracic and cerebral pressures
8. Ultrasound in cardiac arrest
9. Bicarb in cardiac arrest
10. E-CPR
11. Termination of CPR
Take home points
• During arrest is not the time to discuss
nuances, follow the algorithm
• Bystander CPR and early defibrillation is the
most important
• Practice working with teams on scene
• Teach people the basics
• Join goodsam
• Remember the family

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Beyond the protocol

Editor's Notes

  • #2: Not meant to interrupt protocol Might allow us to think outside the box Perhaps where the future of resuscitation is going Sometimes evidence free decision may need to be made when throwing the kitchen sink Not meant for all comers
  • #4: Profound vasoplegia Medical management Is there enough adrenaline? How is the adrenaline delivered periph/central? Aortic catheter placement (reboa/sap) Vasopressin/Noradrenaline/angiotensin II/Calcium/Bicarb/Methylene blue Against guidelines, not evidenced base, should there be a part of the guideline that allows judgment Mechanical REBOA, ECMO, Vasopressin, glucocorticoid, and epinephrine — A randomized trial of 268 consecutive patients with cardiac arrest reported improved survival to hospital discharge with good neurologic status in patients treated initially with the combination of vasopressin, methylprednisolone, and epinephrine (VME group), compared to those treated with placebo plus epinephrine, however, only 25 patients achieved the primary outcome (18 out of 130 [13.9 percent] in VME group versus 7 out of 138 [5.1 percent] in placebo group; odds ratio [OR] 3.28, 95 percent CI 95% CI 1.17-9.20) [69]. Further study is needed before this therapy can be recommended for clinical practice.
  • #6: Driver, resuscitation, use of esmolol after failure of standard CPR to treat patients with refractory VF High level of endogenous and exogenous catecholamines, alpha 1 is good but b1 and b2 may not be so favourable, increase myocardial oxygenation/increase ischaemia/reduce reversion Esmolol: case series evidence only, theory is that VF persistence due to overactive B activity from adrenaline, 500mcg/kg Case series OOHCA and ED arrests with VF/VT initial and 3 shocks given, 3mg adrenaline, 300mg amiodarone given Retrospective, single centre, esmolol previously used removed Outcome: Sustained ROSC for 20min and patient outcomes 90patients, 65 excluded (rosc achieved, wrong amiodarone), 25 analysed, 6 got esmolol and 19 didn’t 66% with esmolol got rosc, 32% in non esmolol group got sustained rosc 50% vs 11% survive to hospital discharge with esmolol Analysis - Small numbers!!! Can’t change practice, Can’t make big statements based on 6 patients, non clinical outcome, single centre Esmolol group explained - Esmolol group 25 min mean prehospital, compared to 42 min prehospital time - Not blinded, may not give esmolol if don’t think its salvageable - Huge bias!!! Good face validity for the study Will this be appropriate if we reduce adrenaline doses? Provides a question for the future
  • #8: Dual sequential defibrillation Rationale: more joules, different vector paths hitting more myocytes, originally described in 1994 5 pts with 7-20 single shocks all reverted with single dsd, 50/50 split in opinion Evidence: only retrospective case reports and case series, tendency to bias towards positive results, no advice beyond shock 5 Negatives: damage defib, needs good CRM What you might do instead Different pad positions eg start AL and change to AP (AL start as out of the way) Increase joules if not a zoll Make sure pads have good contact and are adherent Make sure 4h and 4ts addressed as well as antiarrhythmic Process: change pads on 4th or 5th shock, same operator uses both defib on 5th or 6th shock, doesn’t need to be exact same time Annals of emergency medicine, neil Gerstein, external defib damage associated with attempted synchronised dual dose cardioversion (4 pads ap in this one) Safety issues associated to perform this, A defibrillator damaged with DSD 41 yo male, wide complex, uncompromised, number of attempts resulted in DSD with 2x360j defib, no reversion, coronary cath did, day after showed a life pak failing its automatic self test, zoll defib and lifepak defib Thoughts Doesn’t matter how expensive defib, might want to keep in the arsenal What if you knock out your defibs during? If DSD is done we must check defibs after
  • #9: Stiell IG, Walker RJ et al. Higher Energy Levels for Defibrillation in Out-of-Hospital Cardiac Arrest BIPHASIC Trial. A Randomized Comparison of Fixed Lower Versus Escalating. Circulation. 2007:115. Stiell IG,. Walker RJ et al. Higher Energy Levels for Defibrillation in Out-of-Hospital Cardiac Arrest BIPHASIC Trial. A Randomized Comparison of Fixed Lower Versus Escalating. Circulation. 2007;115. High-energy biphasic truncated exponential waveform vs high current rectilinear biphasic waveform The Stiell study, generally cited as proof, compares only suboptimal dosing with a high-energy waveform starting at 150J vs. a high-energy waveform at escalating energy beginning at 200J. The correct adult dose for high-energy biphasic defibrillation is 200J, 300J, 360J. All this study shows is that if you are going to give multiple shocks with a high-energy defibrillator you ought to be using their protocol of 200J, 300J, and 360J and not reducing the dose below effective levels. ZOLL’s Rectilinear Biphasic waveform delivers significantly more current than high-energy biphasic up to 200J. ZOLL delivers more current at 200J than high-energy defibrillators deliver at 360J. ANZCOR Biphasic waveforms: the default initial energy level for adults should be set at 200J. Other energy levels may be used providing there is relevant clinical data for a specific defibrillator that suggests that an alternative energy level provides adequate shock success (eg. usually greater than 90%) [Class A; LOE II]2 . ANZCOR/ILCOR suggests that if the first shock is not successful and the defibrillator is capable of delivering shocks of higher energy, it is reasonable to increase the energy to the maximum available for subsequent shocks (CoSTR 2015 weak recommendation, very low quality evidence).
  • #10: Fine/low energy VF vs High energy/course VF Fine likely due to poorly perfused myocardium, often go into asystole or PEA after shocking High energy is very irritable, may shock out initially, likely coronary occlusion
  • #11: Transport: after how many shocks, does age matter eg <65, what if there is no mechanical device, what are the guidelines - What is different that the hospital can offer? K, airway if non icp, pci, ecmo Mechanical CPR discussed later, manual cpr in back of ambulance? PCI: more likely if course VF, Resistance from cardiologists due to mortality numbers, does age effect, do you skip other hospitals ECMO: All about getting brain perfusion, Minimum 3 shocks or initial VF rhythm, 20 or 30 minutes cpr, amiodarone…now its refractory
  • #12: For Mechanical: frees up staff, easier access to patient, able to transport, able to screen in pci, scene vibe, frees up situational awareness, manual quality may change, cpr is not interrupted for CPR, angio or ecmo cannulation can continue For Manual: cheaper and just as efficacious, no time to set up, mechanical might be poorer if not aligned, CIRC trial had double rib fractures in mechanical and increased ptx by a third (zoll autopulse), other injuries to liver/spleen, stomach in mechanical group, may not work for certain body times, autopulse radiopaque back board (not for pci) Trials: CIRC (Wik et al, 2014), LINC (Rubertsson et al, 2014), PARAMEDIC (Perkins et al, 2015), CHEER (Stub et al, 2015), ASPIRE, Smekal Gates 2015 et al did a meta-analysis (cheer not included for some reason), 2 trials with autopulse, 3 with lucas Hetrogeniety was large and methodology hard to analyse, lucas only used 40% in mechanical group in paramedic No advantage detected Couper et al (2016) conducted a systematic review of 8 trials and concluded that mechanical chest compression devices may improve patient outcomes when used for in-hospital cardiac arrest  (IHCA), but that the quality of evidence was very low In absence of good data, patient selection comes into paly, when to use Prolonged cpr eg hypothermia, post thrombolysis Few rescuers or unskilled eg prehospital Limited space eg aeromedical, ambulance, radiology ECPR bundle eg CHEER Should it be on the helo?
  • #14: Prognosis: Likely poor prognosis if etco2 <10mmhg despite good compressions, or level at 20min mark - >20 higher chance of rosc, <10 almost no chance, not sure in between Therapeutic: tube position and ventilation effectiveness, CPR effectiveness ROSC: sudden rise in etCO2 suggest ROSC Confounders - Respiratory arrest, PE, disconnected BVM/vent, disconnected co2, dislodged airway
  • #15: ECG in cardiac arrest If STE or new left bundle then it’s a coronary clot and you need pci centre ECG before, during or at rosc might help decide to cardiac centre, qt, arrhythmia, ectopics, brugada, ARVD
  • #16: Prehospital: should they be inserted or just used when they are there? How are they used Targeting diastolic pressures, aiming for a diastolic over 40, remember CPP 15mmg needed, RA pressures 20-30 Better assessment of ROSC than pulse check
  • #17: CVP line femoral: Not that much difference in supine patient, not looking for perfect number just looking for massive numbers Risk is differentiating FA and FV in the heat of the moment ABG: Q6 minutely looking for reversible, Assists successful reversion, Guides ventilation, may want to get pH >7.2 resp compensation etc, will improve haemodynamics, improve rosc, improve PVR, Arterial and venous may be profoundly different eg venous acidaemia and hyperkalaemia Haemodynamic goals Systolic BP: vary rate and depth Diastolic BP: adjust vasopressor, consider additional CVP: bolus, early echo, use for CPP, consider ITD+ACD MAP: ? Optimal target, 70, 80 Ventilation Risk of increasing is increased intrathoracic pressure May increase rate if haemodynamic goals met and pH<7.2, CO2>70 but haemodynamic goals need to be met People ventilate far to fast! Usually around 20-30 Will we target higher co2?  
  • #18: Not uncommon Midaz vs no midaz had worse outcomes in Victoria Fentanyl trialled for non ICP and ketamine for ICP paramedics Resuscitation has a protocol with doses Remember to talk to the patient and explain what’s happening Ask patient to cough, changes impedance, ‘cough CPR’
  • #19: No evidence to support routine pacing in cardiac arrest Randomised controlled trials have failed to show benefit. This absence of P waves and QRS complexes is seen late in arrest when ventricular fibrillation has deteriorated to asystole. Lack of response to pacing is not a failure of the technique of pacing, but rather failure of the hypoxic human heart to respond to pacing with mechanical contractions, despite electrical activity. In the hospital, asystole often represents the final rhythm of a patient whose organs have failed and whose condition has deteriorated. An electrical stimulus in this circumstance usually produces no cardiac response at all, or at the very least, brief episodes of clinically useless PEA.  There are several circumstances in the hospital when asystole appears suddenly and providers are close by to initiate lifesaving pacing: - When the asystole is the result of a primary conduction system problem and ventricular standstill is noted quickly on the monitor in a critical care unit (P waves may still be present) When standstill is drug-induced, e.g., due to procainamide, quinidine, digitalis, beta blockers, verapamil With unexpected circulatory arrest, e.g., due to anesthesia, surgery, angiography, and other therapeutic or diagnostic procedures With reflex vagal standstill: eg bezhold-jarisch reflex, oculocardiac reflex When asystole results following defibrillation, in this last circumstance, it is quick and easy to switch modes on the bedside monitor/defibrillator/pacemaker from defibrillator to noninvasive pacemaker After cardiac surgery or in VAD patients The 2015 European Resuscitation Guidelines advise that in cases of asystole, that the rhythm be checked for P waves, as these may respond to cardiac pacing - Much less likely in unwitnessed
  • #20: Head up resuscitation 45 degrees Reduces venous compression which is what is impairing blood circulation to the brain Not enough clinical data to change practice just yet and remains research Devices assessed by ILCOR and have said not enough evidence to support Impedence threshold device: modulates intrathoracic pressure during inspiration, negative pressure during decompression of the chest Active compression decompression: Like a plunger Interposed abdominal compression: can increase systolic and diastolic BP, myocardial blood flow, and cerebral blood flow Recommendation — Preliminary data suggests that IAC-CPR when used in the in-hospital setting and performed by trained rescuers may be effective, and the ACLS Guidelines state that the technique may be used in this setting. However, the effectiveness of IAC-CPR for achieving improved survival without significant neurologic deficits remains unproven and further study is needed. The ACLS Guidelines state that routine use of ITDs during conventional CPR is not recommended. However, it remains to be determined whether ITDs may benefit particular subgroups of cardiac arrest patients (eg, those treated with active compression-decompression CPR), and therefore, further research with ITDs is justified. The large negative study described above demonstrated equipoise between the ITD and control groups, and therefore we believe it is reasonable for an emergency medical system to use ITDs as part of a well-designed study to better determine their clinical efficacy.
  • #21: Ultrasound in cardiac arrest Prognostication: If you can demonstrate contractility more likely to survive to discharge, Lack of contractility does not equal no survival PEA vs low output state, pulse not always able to be felt Reason trial: Multicenter, Non-randomized, prospective, protocol-driven observational study at 20 hospitals across the United States and Canada, 793 patients Author Conclusion: “Cardiac activity on ultrasound was the variable most associated with survival following cardiac arrest.  Ultrasound during cardiac arrest identifies interventions outside of the standard ACLS algorithm.” PE and Pleural effusion Clinical Take Home Point: The use of bedside ultrasound in PEA/Asystolic cardiac arrest can help identify pathologies that require a specific intervention, used as an adjunct to discontinue resuscitation efforts, and identify cardiac activity that is not appreciated with traditional finger pulse checks. It is unclear from this study whether the use of bedside ultrasound in cardiac arrest is an intervention that improves neurologically intact outcomes. Three rules Don’t use if not going to change Don’t get in the way Don’t over diagnose, look for big pathologies eg tamponade, right heart strain, hypovolaemia, lungs
  • #22: A number of studies and systematic reviews demonstrate increased rosc but increased early mortality Association vs causation is likely at play If not focused, tends to be given in futile arrests therefore a lot of times its used is in a desperate attempt and thus studies don’t show benefit When is it recommended? TCA overdose, hyperkalaemia, ILCOR: combined resp and metabolic acidosis, best treatment is chest compression, some additional benefit by ventilation Bad: abg doesn’t represent tissue pH, generates CO2 rapidly diffuse, worsens intracell acid, negative ino on ischaemic myocardium, large sodium load, left shift
  • #23: Suitable Patients <65 Witnessed VF arrest Bystander CPR Who is not suitable? Elderly Comorbidities e.g. liver, renal failure, severe respiratory disease Advanced malignancies Advanced care directive See STOP criteria >70yrs Unwitnessed >10mins without BLS >60mins since collapse Initial rhythm asystole Organ failure or malignancy No prospect of reversal What happens in the Precannulation phase? (this is essentially a checklist for the ED Consultant) High quality CPR LUCAS Airway secure EtCO2 Expose and shave groins IV access Cath lab aware
  • #24: Compelling reasons to withhold: Adv directive, obvious death, rigor, post mortem lividity, decomp, death declared No prospect of resuscitation: Prolonged arrest and asystole rhythm + estimated time to cpr >20mins Cessation guidelines Pea/asys: 30-45mins als, no compelling reason to continue (20 mins generally consider non survivable for asystole) VF: 45 mins of ALS, can’t be transported with mechanical, no compelling (pupils, agonal/gasping breaths, periods of rosc, youth, absence of comorbidities, etco2 >10, presistant cardiac activity) Remember: Check leads, gain settings and connections, Address all reversible factors General rules No response to ACLS after 20min of efficient resuscitation in the absence of ROSC, a shockable rhythm or reversible causes Pre-existing chronic illness preventing meaningful recovery eg dissmianted ca or nursing home resident Acute illness preventing recovery eg 100% burn, non surv injury, catastrophic tbi with no brain stem reflexes Prehospital Stop CPR if: no rosc, no shocks, not witnessed otherwise transport After the second “ouch” Special circumstances New born baby with no heart rate for 10 minutes Traumatic arrest after interventions performed Exhausted rescuers Prolonged resuscitation Young people with persistent VF until reversible fixed and no therapeutic options Note large Japanese study, paeds, <1% 30d favourable outcome at 42 minutes Hypothermia Asthma, need to correct dynamic hyperinflation Toxicological arrest, full neuro recovery after >4hours possible (asystole may be a direct drug effect that may recover) Thrombolytics given during CPR, should continue up to 2 hours post administration Pregnancy prior to resuscitative caesarean section Drowning: >6 degrees for 30 minutes, <6 degrees up to 66 minutes (selectively cools brain, core might not count) Breaking bad news- SPIKES Setting up: private, involve others, sit, manage/inform of time constraints Perception: before you tell, ask, what do they know, describe events, expectations Invitation: find out how much they want to know, do they want to wait for someone Knowledge: explain wy stopping resuscitation is appropriate, give facts Emotions: address emotions with empathetic responses Strategy and summary: what next How do we get better? Limited training in breaking of bad news in prehospital setting Make three points of contact: introduction relatives, explain what you are doing and maybe your expectation, then if things go poorly can break bad news with someone you have spoken to and have some rapport
  • #25: Focus on the algorithm Bystander CPR and early defibrillation is the most important Work with the teams on scene Teach 2 people Join goodsam It may not be just about survival to discharge: family time, donation etc