INTRA AND POST CARDIAC ARREST MANAGEMENT

It’s not rocket science.. there’s very little“You have to learn the rules of the game. And then you have to play better than anyone else.”

Albert Einstein

“..and sometimes you have to play the game without knowing the rules”

Craig Wallace

Emergency Physician, Modbury Hospital

Setting the sceneHTTP://WWW.YOUTUBE.COM/WATCH?V=ILXJXFB4ZNK

Out of hospital cardiac arrestSurvival to hospital discharge is improving

◦ 47,000 patients in 2010 had 10.4% survival compared with 8.2% in 2006 (Resuscitation, 2015)◦ Improvement is greatest in VF / VT

◦ Probably due to:◦ Increased bystander CPR – compression only

◦ Increased bystander AED use

◦ (similar paramedic response times)

The patient is delivered to the Emergency Department…

Question?How do you use the ACLS guidelines in cardiac arrest management

A. To the letter. It saves me from thinking

B. As a framework for my team but I introduce other interventions as I see fit

C. Not at all. I’m an expert in Emergency Medicine and I know better

D. Not at all. I believe in a Darwinian model of care

E. Other

Goals of peri-arrest managementHow do you hit the target?

Minimize time to ROSC

Minimize post-cardiac arrest syndrome

Seek and treat underlying aetiology

Intra-arrest MINIMIZING TIME TO ROSC

The elephant(s) in the room -

Adrenaline

Amiodarone

Lignocaine

Sodium bicarbonate

Magnesium

Impedance threshold devices

Meta-analysis, Resus 201412250 patients, 9 countries

No difference survival to dischargehigh dose vs std dose vs no dose

Increased survival to admission and ROSC

ILCOR likely to support ongoing use on basis of short term gains

Increased survival to admission and ROSC

Increased survival to admission and ROSC

Very weak evidence

Question?What is your pattern of use for fibrinolytics DURING cardiac arrest?

A. I never use them, they have no known benefit and are likely to be harmful

B. I use them when a patient has an arrest preceded by chest pain

C. I use them routinely, they are as safe as tap water

D. I make it up as I go along on a case by case basis

E. Other

Fibrinolytics in cardiac arrest50-70% of persons of out-of-hospital cardiac arrests (OHCA) have acute myocardial infarction or pulmonary embolism

TROICA trial – prospective randomized trial

Tenecteplase vs no tenecteplase in OHCA◦ 500 patients in each arm

◦ No difference detected in any primary end-point

◦ Study terminated prematurely for lack of effect

Thrombolysis during resuscitation for out-of-hospital cardiac arrestBöttiger et al, NEJM 359(25):2651-62, 2008

So we need to do the simple things well…

AND WHAT DOES THAT MEAN?

Airway and breathing considerationsLaryngeal mask vs. endotracheal tube Manual bag ventilation vs. mechanical

ventilator

CompressionsCessation of chest compressions

◦ Rapid drop in “diastolic” pressure absent coronary perfusion

Minimize interruptions ◦ Intubate during CPR

◦ Femoral arterial line for pulse checks

◦ Look-through cardiac monitors

◦ Hands on defibrillation

Increased depth of compression ◦ Associated with increased survival, Resuscitation 2014

◦ 5mm increase ???

Mechanical CPRMore consistent, don’t stop, minimize the crowd

During transport

BUT

No evidence to show improved survival over standard chest compressions

Identifying the underlying cause4 H’S

Hypoxia

Hypovolaemia◦ AAA

◦ Intraperitoneal bleeding

Hypo / hyper◦ K+ , Na+ , Ca2+

Hypo / hyperthermia

4 T’S

Tension pneumothorax

Tamponade

Thrombosis ◦ Pulmonary or coronary

Toxicology

Novel treatments?Esmolol in refractory VF,

α activation◦ vasoconstriction increased coronary

perfusion pressure

β activation ◦ Increases myocardial oxygen demand

◦ Increases ischaemic injury

◦ Lowers VF threshold

◦ Worsens post-arrest myocardial function

Esmolol has ultra-short t1/2

Has shown promise in animal and human trials

Very small study (6 patients in esmolol arm)

Improved ROSC, survival to discharge and neurological outcome

Use of esmolol after failure of standard cardiopulmonary resuscitation to treat patients with refractory ventricular fibrillationDriver et al., Resuscitation, 85(10):1337-41, 2014

Novel treatments?Vasopressin, steroids and epinephrine

283 patients

14% vs 5% favorable neurological outcomes at discharge

NB this was in hospital cardiac arrest

Evidence in OHCA showed no benefit◦ Timing is likely to be important

Vasopressin, steroids, and epinephrine and neurologically favorable survival after in-hospital cardiac arrest: a randomized clinical trialMentzelopoulos et al. JAMA, 310(3):270-9, 2013

IF NONE OF OUR INTRA -ARREST INTERVENTIONS INCREASE SURVIVAL TO DISCHARGE

But help in achieving ROSC

WE ARE TRYING TO ACHIEVE ROSC IN THE HOPE THAT OUR POST -ARREST CARE HAS IMPROVED OR WILL IMPROVE DOWN THE ROAD

Post arrestMINIMIZING POST-CARDIAC ARREST SYNDROME

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Post cardiac arrest syndrome

◦ Anoxic brain injury

◦ Arrest related myocardial dysfunction

◦ Systemic ischaemia / reperfusion response

◦ Persistent precipitating aetiology

OxygenationHypoxia is bad

Severe hyperoxia is possibly bad◦ PaO2 > 300mmHg

◦ Associated with decreases survival to discharge

◦ Worse organ function at 24 hours

◦ Other studies have not found this association

Moderate hyperoxia doesn’t have this association

Severe hyperoxia in Cardiac Arrest Survivors is Associated with Worse Outcomes. Elmer et al., Intensive Care Medicine, 41: 49

VentilationHypocapnia is bad cerebral vasoconstriction and decreased cerebral blood flow

Mild hypercapnia may be associated with improved outcomes

Lung injury prevention ventilation should be employed

◦ 5-7ml/kg (ideal body weight) as per ARDS Net

Question?Do you routinely use neuromuscular blockers post cardiac arrest?

A. Never, They are associated with critical illness polyneuropathy

B. Always, to help prevent shivering and rewarming

C. Only when the patient is fighting the ventilator

D. Never, I use fighting the ventilator as a sign of neurological function

E. Other

Neuromuscular blockade (NMB)Reduces metabolic demand and global oxygen consumption

Improves pulmonary gas exchange

Prevents ventilator dyssynchrony protects against episodic rises in intracranial pressure

Prevents shivering and re-warming

Small study (111 patients) showing improved survival with NMB for 24 hrs vs no NMB◦ 74% vs 41% survival

Continuous neuromuscular blockade is associated with decreased mortality in post-cardiac arrest patients.Salciccioli et al, Resuscitation 84(12):1728-33, 2013

Circulatory supportAim to maintain coronary and cerebral blood flow

Cerebral autoregulation impaired◦ Blood flow may decline when MAP <80-100mmHg

Optimal targets remain unclear◦ Sepsis targets have suggested MAP>65mmHg

◦ Higher targets may be better in post arrest

◦ MAP 70 - 85 have been associated with better outcome

Cerebral blood flow

Hemodynamic targets during therapeutic hypothermia after cardiac arrest: A prospective observational study.Ameloot K et al. Resuscitation, 91:56-62 2015

Targeted temperature managementStudy No. of pts Target T°C Survival % Good neuro outcome %

HACA, 2002 275 32-34 59 vs 45 55 vs 39

Bernard, 2002 77 33 49 vs 32 49 vs 26

TTM, 2013 939 33 vs 36 50 vs 48 54 vs 52*

*Death or poor outcome at 180 days

Inducing hypothermia is out

BUT preventing fever is paramount

Targeted temperature management at 33°C versus 36°C after cardiac arrestNielsen et al. NEJM, 369(23):2197-206, 2013

Myocardial dysfunction – a waterfall effectPrimary underlying myocardial pathology

◦ Acute coronary syndrome

◦ PE

◦ Primary dysrhythmia

Metabolic / pharmacologic induced◦ Metabolic acidosis

◦ Catecholamines

Systemic inflammation◦ Cytokine induced myocardial depression

QuestionIn all cardiac arrests with ROSC, but remaining comatose, I get the patient to the cath lab

A. Immediately, this is life-saving and I’m on the phone to the interventional cardiologist

B. Delayed but less than 24 hours, while important I don’t want to wake the cardiologist up

C. Delayed but I’m not pushing it as there are bigger things for the patient to survive

D. Not at all, the is no role

E. Other

Cath lab – feeding the coronary tree of life?It has face validity

ACS is the leading cause of cardiac arrest◦ A culprit coronary lesion will exist in a percentage of

these

Clear data supporting PCI for STEMI◦ Time critical

Intervention in NSTEMI is less time critical◦ Except very high risk patients (GRACE scores)

Cath lab in NSTEMIImproved survival to discharge with good neurological outcome (60% vs 40%)

Interestingly comparing PCI with no PCI had same survival

◦ Suggests other therapeutic benefit to being in a cath lab◦ Haemodynamic evaluation and support

◦ Identify structural defects

◦ Temporary pacing

◦ Pulmonary embolectomy

◦ Pressor / vasodilation titration

Early cardiac catheterization is associated with improved survival in comatose survivors of cardiac arrest without STEMIHollenbeck et al., Resuscitation, 85(1): 88-95, 2014

Patient selection – how?STEMI by ECG after cardiac arrest

◦ Sensitivity 77%, Specificity 69%

◦ i.e. 23% false negatives, 31% false positives

Myocardial conduction is significantly deranged in the post-arrest metabolic milieu

At least 30% of cardiac arrest patients are not related to ACS and may not benefit from the cath lab

The accuracy of an out-of-hospital 12-lead ECG for the detection of ST-elevation myocardial infarction immediately after resuscitation. Müller, Ann Em Med 52(6): 658-664

Cardiac Arrest: A Treatment Algorithm for Emergent Invasive Cardiac Procedures in the Resuscitated Comatose

Patient. Rab et al. JACC July 2015; 66 (1): 62 – 73

Systemic inflammation from ischaemia or reperfusionAdditional haemodynamic compromise from

◦ Cytokine induced myocardial depression

◦ Vasoplegia

◦ Hypovolaemia

◦ Procoagulation

Extrapolation of Sepsis “bundles”◦ Glycemic control

◦ Antibiotics◦ There is some weak evidence about less pneumonia if used prophylactically

◦ (Targeted haemodynamics) – early and aggressive

ECMO incardiacarrest

STRETCHING THE BOUNDARIES

QuestionIf I could have the resources for ECMO use in cardiac arrest, I would

A. Use it on all-comers, chance of life comes at no cost

B. Use it on selected individuals, though I don’t exactly know who they are yet

C. Use it on nobody, its unethical to provide such an intense resource to so few

D. What does ECMO stand for again?

Extra Corporeal Membrane Oxygenation - an example protocol in OHCABased on CHEER (CPR mechanically delivered, Hypothermia, ECMO, Emergency Reperfusion)

Paramedic callout ◦ 30 minutes CPR with no ROSC

◦ Transport to ED with MECHANICAL CPR device

◦ (induction of hypothermia with ice cold saline)

◦ Standard CPR interventions

Arrival ED◦ Confirm refractory arrest

◦ Continue to ECMO establishment

Veno-Arterial ECMO

1. Placement of ECMO cannulas◦ Venous 17-21 F femoral vein to entry of right

atrium

◦ Arterial 15-19F femoral artery 15-20cm insertion length

3. Attach to centrifugal pump◦ Oxygenated, anticoagulated

◦ Note flow is retrograde

IVC

ECMO protocol continuedECMO established

Anticoagulation with UFH

Adrenaline infusion to titrate MAP to 70mmHg

Transfer to manage underlying cause◦ PE CTPA + thrombolysis / embolectomy

◦ Coronary occlusion Coronary angiogram +/- PCI

Backflow cannula for femoral arterial flow – may need theatre for this

Palliation for poor neurological prognosis (timing?) or uncontrollable bleeding

ECMO outcomes- observational dataMultinational experience

◦ San Diego – 127 pts, 26% survival – in-hospital arrests

◦ Harvard - ELSO database 27% survival – in-hospital arrests

◦ Seoul – 59 cases, 33% survival, 80% “acceptable brains” – in-hospital arrests

◦ Japan - ECPR vs cCPR : a prospective observational study 60 patients – Resus, 2015◦ higher survival with good neuro outcome 8/20 vs 3/40

◦ Paris – OHCA, 4% survival◦ Japan

◦ OHCA, 86 patients, 29% 30-day survival, favourable neuro outcome 24%

◦ Included intra-arrest PCI

◦ Australia (CHEER) feasibility study◦ 26 patients combined OHCA and IHCA; 5/11 OHCA survived with

full neurological recovery

Times to ROSC were longer but despite this there were good

neurological outcomes in a number of the studies

IssuesComplications are common (up to 70%)

◦ Bleeding

◦ Infection

◦ Thromboembolism ◦ Limb ischemia

◦ Stroke

Evidence based on observational studies only◦ Selection bias

◦ IHCA vs OHCA or combined study

Ethical dilemmas◦ Benefits and risks

◦ Consent◦ Does presumptive consent apply to eCPR

◦ Appropriate use

◦ Cost-effectiveness

Summary

Intra-arrest◦ Optimize oxygenation

◦ Avoid hyperventilation

◦ Minimize compression interruptions

◦ No new medicines for prime time as yet

Post-arrest◦ Avoid hyperoxia

◦ Aim for normal to slightly raised Pa CO2

◦ Aim for higher MAP 70-85mmHg

◦ Avoid fever

◦ Consider early transfer to cath lab especially if ACS suspected

◦ ECMO – is still defining its position

ACLS guidelines provide a framework for cardiac arrest management but can be pushed towards more cutting edge care

Take home message?.BOTSWANA IS AN EXCELLENT PLACE AS A CAMPING HOLIDAY